Relevant bibliographies by topics / Autophagy

Academic literature on the topic 'Autophagy'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Autophagy"

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Sakai, Shinsuke, Takeshi Yamamoto, Yoshitsugu Takabatake, Atsushi Takahashi, Tomoko Namba-Hamano, Satoshi Minami, Ryuta Fujimura, et al. "Proximal Tubule Autophagy Differs in Type 1 and 2 Diabetes." Journal of the American Society of Nephrology 30, no. 6 (April 30, 2019): 929–45. http://dx.doi.org/10.1681/asn.2018100983.

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BackgroundEvidence of a protective role of autophagy in kidney diseases has sparked interest in autophagy as a potential therapeutic strategy. However, understanding how the autophagic process is altered in each disorder is critically important in working toward therapeutic applications.MethodsUsing cultured kidney proximal tubule epithelial cells (PTECs) and diabetic mouse models, we investigated how autophagic activity differs in type 1 versus type 2 diabetic nephropathy. We explored nutrient signals regulating starvation-induced autophagy in PTECs and used autophagy-monitoring mice and PTEC-specific autophagy-deficient knockout mice to examine differences in autophagy status and autophagy’s role in PTECs in streptozotocin (STZ)-treated type 1 and db/db type 2 diabetic nephropathy. We also examined the effects of rapamycin (an inhibitor of mammalian target of rapamycin [mTOR]) on vulnerability to ischemia-reperfusion injury.ResultsAdministering insulin or amino acids, but not glucose, suppressed autophagy by activating mTOR signaling. In db/db mice, autophagy induction was suppressed even under starvation; in STZ-treated mice, autophagy was enhanced even under fed conditions but stagnated under starvation due to lysosomal stress. Using knockout mice with diabetes, we found that, in STZ-treated mice, activated autophagy counteracts mitochondrial damage and fibrosis in the kidneys, whereas in db/db mice, autophagic suppression jeopardizes kidney even in the autophagy-competent state. Rapamycin-induced pharmacologic autophagy produced opposite effects on ischemia-reperfusion injury in STZ-treated and db/db mice.ConclusionsAutophagic activity in PTECs is mainly regulated by insulin. Consequently, autophagic activity differs in types 1 and 2 diabetic nephropathy, which should be considered when developing strategies to treat diabetic nephropathy by modulating autophagy.
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Gordon, P. B., H. Høyvik, and P. O. Seglen. "Prelysosomal and lysosomal connections between autophagy and endocytosis." Biochemical Journal 283, no. 2 (April 15, 1992): 361–69. http://dx.doi.org/10.1042/bj2830361.

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In isolated rat hepatocytes electroloaded with [14C]sucrose, autophaged sugar accumulated in lysosomes under control conditions, and in prelysosomal autophagic vacuoles (amphisomes) in the presence of asparagine, an inhibitor of autophagic-lysosomal fusion. Endocytic uptake of the sucrose-cleaving enzyme invertase resulted in rapid and complete degradation of autophaged sucrose in both amphisomes and lysosomes. Pre-accumulated sucrose was degraded equally well in both compartments, regardless of amphisomal-lysosomal flux inhibition by asparagine, suggesting that endocytic entry into the autophagic pathway can take place both at the lysosomal and at the amphisomal level. The completeness of sucrose degradation by endocytosed invertase furthermore indicates that all lysosomes involved in autophagy can also engage in endocytosis. Endocytosed invertase reached the amphisomes even when autophagy was blocked by 3-methyladenine, and autophaged sucrose reached this compartment even when endocytic influx was blocked by vinblastine, suggesting that amphisomes may exhibit some degree of permanence independently of either pathway.
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Chueh, Kuang-Shun, Jian-He Lu, Tai-Jui Juan, Shu-Mien Chuang, and Yung-Shun Juan. "The Molecular Mechanism and Therapeutic Application of Autophagy for Urological Disease." International Journal of Molecular Sciences 24, no. 19 (October 4, 2023): 14887. http://dx.doi.org/10.3390/ijms241914887.

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Autophagy is a lysosomal degradation process known as autophagic flux, involving the engulfment of damaged proteins and organelles by double-membrane autophagosomes. It comprises microautophagy, chaperone-mediated autophagy (CMA), and macroautophagy. Macroautophagy consists of three stages: induction, autophagosome formation, and autolysosome formation. Atg8-family proteins are valuable for tracking autophagic structures and have been widely utilized for monitoring autophagy. The conversion of LC3 to its lipidated form, LC3-II, served as an indicator of autophagy. Autophagy is implicated in human pathophysiology, such as neurodegeneration, cancer, and immune disorders. Moreover, autophagy impacts urological diseases, such as interstitial cystitis /bladder pain syndrome (IC/BPS), ketamine-induced ulcerative cystitis (KIC), chemotherapy-induced cystitis (CIC), radiation cystitis (RC), erectile dysfunction (ED), bladder outlet obstruction (BOO), prostate cancer, bladder cancer, renal cancer, testicular cancer, and penile cancer. Autophagy plays a dual role in the management of urologic diseases, and the identification of potential biomarkers associated with autophagy is a crucial step towards a deeper understanding of its role in these diseases. Methods for monitoring autophagy include TEM, Western blot, immunofluorescence, flow cytometry, and genetic tools. Autophagosome and autolysosome structures are discerned via TEM. Western blot, immunofluorescence, northern blot, and RT-PCR assess protein/mRNA levels. Luciferase assay tracks flux; GFP-LC3 transgenic mice aid study. Knockdown methods (miRNA and RNAi) offer insights. This article extensively examines autophagy’s molecular mechanism, pharmacological regulation, and therapeutic application involvement in urological diseases.
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López-Alonso, Inés, Alina Aguirre, Adrián González-López, Álvaro F. Fernández, Laura Amado-Rodríguez, Aurora Astudillo, Estefanía Batalla-Solís, and Guillermo M. Albaiceta. "Impairment of autophagy decreases ventilator-induced lung injury by blockade of the NF-κB pathway." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 12 (June 15, 2013): L844—L852. http://dx.doi.org/10.1152/ajplung.00422.2012.

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Excessive lung stretch triggers lung inflammation by activation of the NF-κB pathway. This route can be modulated by autophagy, an intracellular proteolytic system. Our objective was to study the impact of the absence of autophagy in a model of ventilator-induced lung injury. Mice lacking Autophagin-1/ATG4B ( Atg4b −/−), a critical protease in the autophagic pathway, and their wild-type counterparts were studied in baseline conditions and after mechanical ventilation. Lung injury, markers of autophagy, and activation of the inflammatory response were evaluated after ventilation. Mechanical ventilation increased autophagy and induced lung injury in wild-type mice. Atg4b −/− animals showed a decreased lung injury after ventilation, with less neutrophilic infiltration than their wild-type counterparts. As expected, autophagy was absent in mutant animals, resulting in the accumulation of p62 and ubiquitinated proteins. Activation of the canonical NF-κB pathway was present in ventilated wild-type, but not Atg4b-deficient, animals. Moreover, these mutant mice showed an accumulation of ubiquitinated IκB. High-pressure ventilation partially restored the autophagic response in Atg4b −/− mice and abolished the differences between genotypes. In conclusion, impairment of autophagy results in an ameliorated inflammatory response to mechanical ventilation and decreases lung injury. The accumulation of ubiquitinated IκB may be responsible for this effect.
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Zolotova, S. A., and S. V. Palyanov. "The role of autophagy in cardiac damage." Scientific Bulletin of the Omsk State Medical University 3, no. 1 (2023): 71–83. http://dx.doi.org/10.61634/2782-3024-2023-9-71-83.

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Autophagy is one of the mechanisms ensuring cell homeostasis on the one hand, and on the other hand, it is a way of utilizing damaged cell structures through their autolysis in the autophagosome for reuse in cell metabolism. Autophagy is usually considered as an adaptive process allowing cells to survive under conditions of stress, nutrient deficiency and hypoxia. However, under certain circumstances autophagy can be the cause of cell death. Cell death accompanied by autophagy activation and autophagosome accumulation has been classified as programmed cell death type II. However, compared to detailed information on the adaptive role of autophagy, its involvement in cell death has been poorly understood. Autophagic cell death can be divided into two groups, namely: (1) autophagic cell death with increased autophagy activity; (2) autophagic cell death with decreased autophagy processes. In the first scenario, autophagy is excessively activated, causing uncontrolled autolysis of cellular structures and cell death. A similar scenario is observed in cell death caused by excessive degradation of damaged organelles in lysosomes. Of particular interest is a specific form of autophagy in which damaged mitochondria are excessively eliminated from the cell - mitophagy. Autophagic cell death is characteristic of diabetic cardiomyopathy. The second variant, characterized by reduced autophagy processes, is observed in doxorubicin-induced cardiomyopathy, autophagy during ischemia/reperfusion and autophagic cell death in lysosomal accumulation diseases. In this scenario, the final step of autophagy is usually disrupted, and an imbalance between autophagosome formation and lysosomal activity leads to massive autophagosome accumulation, which subsequently causes cellular dysfunction and death. Dysregulation of autophagy causes a unique form of cell death, called autosis, with certain morphological and biochemical features that differ from other forms of cell death, such as apoptosis and necrosis. In autosis, Na+/K+ ATPase plays a special role, which by physically interacting with Beclin 1 can promote autophagic cell death. The principles of therapeutic intervention aimed at preventing autophagic death of cardiomyocytes depend on the specific mechanisms of autophagy. For example, the use of Na+/K+-ATPase inhibitors, such as cardiac glycosides, provides a cardioprotective effect by inhibiting autophagy, while the use of trehalose and 3,4-dimethoxychalcon, can optimize autophagy processes and reduce the intensity of excessive autophagosome accumulation. Thus, the study of mechanisms of autophagy and search for new approaches in pharmacocorrection and pharmacoprophylaxis of autophagic cell death are actual directions of modern scientific research. The aim of the review is to present the concept of autophagic cell death in some heart diseases.
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Yang, Fan, Haoran Hu, Wenjing Yin, Guangyi Li, Ting Yuan, Xuetao Xie, and Changqing Zhang. "Autophagy Is Independent of the Chondroprotection Induced by Platelet-Rich Plasma Releasate." BioMed Research International 2018 (July 24, 2018): 1–11. http://dx.doi.org/10.1155/2018/9726703.

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Background. Platelet-rich plasma (PRP) has been shown to be a promising therapeutic agent against osteoarthritis (OA), whereas its chondroprotection mechanism is not fully elucidated. Autophagy is considered an important biological process throughout the development of OA. Therefore, the objective of the present study is to investigate the role of autophagy in the chondroprotection and compare the effects of releasate between L-PRP and P-PRP. Methods. PRP were prepared from rat blood. Rat chondrocytes pretreated in the presence or absence of interleukin-1 beta (IL-1β) were incubated with PRP releasate. The expressions of OA-related genes and autophagy-related genes were determined by RT-PCR and western blot, respectively. Autophagic bodies were assessed by transmission electron microscopy and the autophagy flux was monitored under the confocal microscopy. The effect of PRP on autophagy was further investigated in the milieu of autophagy activator, rapamycin, or autophagy inhibition by downregulation of Atg5. The effect of PRP on cartilage repair and autophagy was also evaluated in an OA rat model. Results. In vitro, PRP releasate increased the expression of the anabolic genes, COL2 and Aggrecan, and decreased the expression of the catabolic genes, whereas the expression of autophage markers, Atg5 and Beclin-1, as well as the ratio of LC3 II/LC3 I, was not significantly altered in normal or IL-1β-treated chondrocytes. Similar expression pattern was found following the activation (rapamycin) or inhibition (Atg5 silencing) of autophagy. In vivo, PRP releasate ameliorated posttraumatic cartilage degeneration while the expression of LC3 was comparable to that in the vehicle treatment group. Conclusions. PRP releasate promoted the anabolic gene expression, relieved inflammatory stress in chondrocytes, and ameliorated cartilage degeneration, but autophagy was independent of these processes.
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Li, Jiarou, and Hongliang Wang. "Autophagy-dependent ferroptosis in infectious disease." Journal of Translational Internal Medicine 11, no. 4 (December 1, 2023): 355–62. http://dx.doi.org/10.2478/jtim-2023-0099.

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Abstract Autophagy is the initial defense response of the host against pathogens. Autophagy can be either non-selective or selective. It selectively targets the degradation of autophagic substrates through the sorting and transportation of autophagic receptor proteins. However, excessive autophagy activity will trigger cell death especially ferroptosis, which was characterized by the accumulation of lipid peroxide and free iron. Several certain types of selective autophagy degrade antioxidant systems and ferritin. Here, we summarized the latest researches of autophagy in infection and discuss the regulatory mechanisms and signaling pathways of autophagy-dependent ferroptosis.
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Ko, Su-Hyuk, Gilberto Gonzalez, Zhijie Liu, and Lizhen Chen. "Axon Injury-Induced Autophagy Activation Is Impaired in a C. elegans Model of Tauopathy." International Journal of Molecular Sciences 21, no. 22 (November 13, 2020): 8559. http://dx.doi.org/10.3390/ijms21228559.

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Autophagy is a conserved pathway that plays a key role in cell homeostasis in normal settings, as well as abnormal and stress conditions. Autophagy dysfunction is found in various neurodegenerative diseases, although it remains unclear whether autophagy impairment is a contributor or consequence of neurodegeneration. Axonal injury is an acute neuronal stress that triggers autophagic responses in an age-dependent manner. In this study, we investigate the injury-triggered autophagy response in a C. elegans model of tauopathy. We found that transgenic expression of pro-aggregant Tau, but not the anti-aggregant Tau, abolished axon injury-induced autophagy activation, resulting in a reduced axon regeneration capacity. Furthermore, axonal trafficking of autophagic vesicles were significantly reduced in the animals expressing pro-aggregant F3ΔK280 Tau, indicating that Tau aggregation impairs autophagy regulation. Importantly, the reduced number of total or trafficking autophagic vesicles in the tauopathy model was not restored by the autophagy activator rapamycin. Loss of PTL-1, the sole Tau homologue in C. elegans, also led to impaired injury-induced autophagy activation, but with an increased basal level of autophagic vesicles. Therefore, we have demonstrated that Tau aggregation as well as Tau depletion both lead to disruption of injury-induced autophagy responses, suggesting that aberrant protein aggregation or microtubule dysfunction can modulate autophagy regulation in neurons after injury.
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Kasprowska-Liśkiewicz, Daniela. "The cell on the edge of life and death: Crosstalk between autophagy and apoptosis." Postępy Higieny i Medycyny Doświadczalnej 71 (September 21, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.4672.

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Recently, the crosstalk between autophagy and apoptosis has attracted broader attention. Basal autophagy serves to maintain cell homeostasis, while the upregulation of this process is an element of stress response that enables the cell to survive under adverse conditions. Autophagy may also determine the fate of the cell through its interactions with cell death pathways. The protein networks that control the initiation and the execution phase of these two processes are highly interconnected. Several scenarios for the crosstalk between autophagy and apoptosis exist. In most cases, the activation of autophagy represents an attempt of the cell to cope with stress, and protects the cell from apoptosis or delays its initiation. Generally, the simultaneous activation of pro-survival and pro-death pathways is prevented by the mutual inhibitory crosstalk between autophagy and apoptosis. But in some circumstances, autophagy or the proteins of the core autophagic machinery may promote cellular demise through excessive self-digestion (so-called “autophagic cell death”) or by stimulating the activation of other cell death pathways. It is controversial whether cells actually die via autophagy, which is why the term “autophagic cell death” has been under intense debate lately. This review summarizes the recent findings on the multilevel crosstalk between autophagy and apoptosis in aspects of common regulators, mutual inhibition of these processes, the stimulation of apoptosis by autophagy or autophagic proteins and finally the role of autophagy as a death-execution mechanism.
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Körholz, Katharina, Johannes Ridinger, Damir Krunic, Sara Najafi, Xenia F. Gerloff, Karen Frese, Benjamin Meder, et al. "Broad-Spectrum HDAC Inhibitors Promote Autophagy through FOXO Transcription Factors in Neuroblastoma." Cells 10, no. 5 (April 24, 2021): 1001. http://dx.doi.org/10.3390/cells10051001.

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Depending on context and tumor stage, deregulation of autophagy can either suppress tumorigenesis or promote chemoresistance and tumor survival. Histone deacetylases (HDACs) can modulate autophagy; however, the exact mechanisms are not fully understood. Here, we analyze the effects of the broad-spectrum HDAC inhibitors (HDACi) panobinostat and vorinostat on the transcriptional regulation of autophagy with respect to autophagy transcription factor activity (Transcription factor EB—TFEB, forkhead boxO—FOXO) and autophagic flux in neuroblastoma cells. In combination with the late-stage autophagic flux inhibitor bafilomycin A1, HDACis increase the number of autophagic vesicles, indicating an increase in autophagic flux. Both HDACi induce nuclear translocation of the transcription factors FOXO1 and FOXO3a, but not TFEB and promote the expression of pro-autophagic FOXO1/3a target genes. Moreover, FOXO1/3a knockdown experiments impaired HDACi treatment mediated expression of autophagy related genes. Combination of panobinostat with the lysosomal inhibitor chloroquine, which blocks autophagic flux, enhances neuroblastoma cell death in culture and hampers tumor growth in vivo in a neuroblastoma zebrafish xenograft model. In conclusion, our results indicate that pan-HDACi treatment induces autophagy in neuroblastoma at a transcriptional level. Combining HDACis with autophagy modulating drugs suppresses tumor growth of high-risk neuroblastoma cells. These experimental data provide novel insights for optimization of treatment strategies in neuroblastoma.
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Dissertations / Theses on the topic "Autophagy"

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Vigié, Pierre. "Mitochondrial quality control : roles of autophagy, mitophagy and the proteasome." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0202/document.

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La mitophagie, la dégradation sélective des mitochondries par autophagie, est impliquée dans l’élimination des mitochondries endommagées ou superflues et requiert des régulateurs et protéines spécifiques. Chez la levure, Atg32, localisée dans la membrane externe mitochondriale, interagit avec Atg8, et permet le recrutement des mitochondries et leur séquestration à l’intérieur des autophagosomes. Atg8 est conjuguée à de la phosphatidyléthanolamine et est ainsi ancrée aux membranes du phagophore et des autophagosomes. Chez la levure, plusieurs voies de synthèse de PE existent mais leur contribution dans l’autophagie et la mitophagie est inconnue. Dans le premier chapitre, nous avons étudié la contribution des différentes enzymes de synthèse de PE, dans l’induction de l’autophagie et la mitophagie et nous avons démontré que Psd1, la phosphatidylsérine décarboxylase mitochondriale, est impliquée dans la mitophagie seulement en condition de carence azotée alors que Psd2, localisée dans les membranes vacuolaires, endosomales et de l’appareil de Golgi, est nécessaire en phase stationnaire de croissance. Dans le second chapitre, la relation entre Atg32, la mitophagie et le protéasome a été étudiée. Nous avons démontré que l’activité du promoteur d’ATG32 et la quantité de protéine Atg32 exprimée sont inversement régulées. En phase stationnaire de croissance, l’inhibition du protéasome empêche la diminution de l’expression d’Atg32 et la mitophagie est stimulée. Nos données montrent ainsi que la quantité d’Atg32 est reliée à l’activité du protéasome et que cette protéine pourrait être ubiquitinylée. Dans le troisième chapitre, nous nous sommes intéressés au rôle potentiel de Dep1, un composant du complexe nucléaire Rpd3 d’histones déacétylases, dans la mitophagie. Dans nos conditions, Dep1 semble être mitochondriale et elle est impliquée dans la régulation de la mitophagie. BRMS1L (Breast Cancer Metastasis suppressor 1-like) est l’homologue de Dep1 chez les mammifères. Cette protéine possède un rôle anti-métastatique dans des lignées de cancer du sein. Nous avons trouvé que l’expression de BRMS1L augmente en présence de stimuli pro-mitophagie
Mitophagy, the selective degradation of mitochondria by autophagy, is implicated in the clearance of superfluous or damaged mitochondria and requires specific proteins and regulators. In yeast, Atg32, an outer mitochondrial membrane protein, interacts with Atg8, promoting mitochondria recruitment to the phagophore and their sequestration within autophagosomes. Atg8 is anchored to the phagophore and autophagosome membranes thanks to phosphatidylethanolamine (PE). In yeast, several PE synthesis pathways have been characterized, but their contribution to autophagy and mitophagy is unknown. In the first chapter, we investigated the contribution of the different enzymes responsible for PE synthesis in autophagy and mitophagy and we demonstrated that Psd1, the mitochondrial phosphatidylserine decarboxylase, is involved in mitophagy induction only in nitrogen starvation, whereas Psd2, located in vacuole/Golgi apparatus/endosome membranes, is required preferentially for mitophagy induction in stationary phase of growth. In the second chapter, we were interested in the relationship between Atg32, mitophagy and the proteasome. We demonstrated that ATG32 promoter activity and protein expression are inversely regulated. During stationary phase of growth, proteasome inhibition abolishes the decrease in Atg32 expression and mitophagy is enhanced. Our data indicate that Atg32 protein is regulated by the proteasome activity and could be ubiquitinated. In the third chapter, we investigated the involvement of Dep1, a member of the nuclear Rpd3L histone deacetylase complex, in mitophagy. In our conditions, Dep1 seems to be located in mitochondria and is a novel effector of mitophagy both in nitrogen starvation and stationary phase of growth. BRMS1L (Breast Cancer Metastasis suppressor 1-like) is the mammalian homolog of Dep1 and has been described in breast cancer metastasis suppression. We found that BRMS1L protein expression increases upon pro-mitophagy stimuli
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Akinduro, Olufolake A. E. "Autophagy in epidermis." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8703.

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Organ‐transplant recipients (OTRs) on a new class of immunosuppressants, rapamycin and its analogues, have reduced cutaneous Squamous Cell Carcinomas (cSCCs). Rapamycin, an mTORC1 inhibitor, is also a known autophagy inducer in experimental models. Autophagy, which literally means self‐eating, is a cell survival mechanism but can also lead to cell death. Therefore, the main hypothesis behind this work is that rapamycin prevents epidermal tumourigenesis by either affecting epidermal mTOR regulation of autophagy and/or selectively affecting epidermal AKT isoform activity. Epidermal keratinocytes move from the proliferating basal layer upwards to the granular layers where they terminally differentiate, forming a layer of flattened, anucleate cells or squames of the cornified layer which provides an essential environmental barrier. However, epidermal terminal differentiation, a specialised form of cell death involving organelle degradation, is poorly understood. The work presented in this thesis shows that analysis of the autophagy marker expression profile during foetal epidermal development, indicates autophagy is constitutively active in the terminally differentiating granular layer of epidermis. Therefore, I hypothesize that autophagy is a mechanism of organelle degradation during terminal differentiation of granular layer keratinocytes. In monolayer keratinocytes, activation of terminal differentiation is accompanied by autophagic degradation of nuclear material, nucleophagy. This suggests that constitutive autophagy is a pro‐death mechanism required for terminal differentiation. In cultured keratinocytes and in epidermal cultures, rapamycinmediated mTORC1 inhibition strongly increases AKT1 activity as well as up‐regulates constitutive granular layer autophagy promoting terminal differentiation. Therefore, autophagy is an important fundamental process in keratinocytes which may be the mechanism by which terminally differentiating keratinocytes of the epidermal granular layer degrade their organelles required for barrier formation. This may have implications for the treatment of patients with barrier defects like psoriasis. In immunosuppressed OTRs, rapamycin may promote epidermal autophagy and AKT1 activity adding to its anti‐tumourigenic properties.
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Malik, Shoaib Ahmad. "Crosstalk Between Apoptosis and Autophagy : BH3 Mimetics Activate Multiple Pro-Autophagic Pathways." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T044/document.

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La macro-autophagie est une voie catabolique conservée dans l’évolution permettant la dégradation des organites endommagés ou vieux, des protéines à longue durée de vie ou agrégées et des portions du cytosol pour le recyclage métabolique afin de maintenir l'homéostasie cellulaire. L'absence d'autophagie est fréquemment observée dans de nombreuses pathologies incluant les cancers et les maladies neurodégénératives. Beclin 1, un suppresseur de tumeur,est une protéine clé dans la régulation de l’autophagie et participe à la nucléation de l’autophagosome. Beclin 1 est une protéine “BH3-only” pouvant interagir avec le site de fixation au domaine BH3 présent dans la protéine Bcl-2 et ses homologues. Cette interaction inhibe l’autophagie. Certains agents pharmacologiques tels qu’ABT737, appelés«BH3 mimetics», occupent le site de fixation du domaine BH3 de façon compétitive pour perturber l'interaction inhibitrice entre Beclin 1 et Bcl-2/Bcl-XL. Ceci permet à Beclin 1 de maintenir l’activité classe IIIphosphatidylinositol-3-kinase de Vps34 pour la formation du phagophore. L'autophagie est un processus finement régulé par de nombreux complexes protéiques. Les senseurs de la charge énergétique comme l’AMP-dependant kinase(AMPK), la cible mammalienne de la rapamycine (mTOR), la Sirtuin1 (SIRT1) ou les voies d’intégration du stress telles que celles impliquant l'inhibiteur des kinases NF-κB (IκBα) (IKK) et le suppresseur de tumeur p53, ont tous un impact majeur dans la régulation de l'autophagie. Dans de nombreux paradigmes de stimulation autophagique, ils semblent tous agir en amont de la dissociation Beclin 1-Bcl-2. Nos résultats révèlent qu’ABT737 stimule plusieurs voies pro-autophagiques pour obtenir une efficacité optimale. Ces résultats placent la SIRT1, AMPK / mTOR, HDM2et IKK en aval de la dissociation du complexe Beclin 1-Bcl-2. Cette étude démontre que les BH3-mimetics activent des voies multiples de stimulation de l’autophagie, peut-être en raison du degré élevé de connectivité qui existe entre les complexes protéiques de régulation de l’autophagie. Cela signifie qu’un effet spécifique sur l’interactome de Beclin 1 peut affecter d'autres voies dans le réseau du contrôle autophagique. Ces voies ne semblent pas suivre une hiérarchie linéaire, mais doivent être plutôt interconnectées dans un circuit complexe dans lequel la stimulation de l'autophagie par des déclencheurs physiologiques (tels que la carence en nutriments ou le stress des organites) induit un ensemble de changements intimement liés et impliqués dans une boucle de régulation positive qui constituerait un ensemble indissociable composant l’«autophagy switch»
Macro-autophagy is a conserved catabolic pathway that culminates in the degradation of old/damaged organelles,long-lived/aggregated proteins and portions of the cytosol for metabolic recycling to maintain cellular homeostasis.The absence of autophagy is frequently observed in many pathologies including cancers and neurodegenerative diseases. Beclin 1, a bona fide tumour suppressor, is the key autophagy regulatory protein that participates in autophagosome nucleation. Infect, Beclin 1 is a BH3-only protein that can interacts with the BH3 receptor domain contained within Bcl-2 and its homologues. This interaction functions as a inhibitory check on autophagy. Some pharmacological agents such as ABT737, referred to as ‘BH3 mimetics’, occupy the BH3-binding grooves to competitively disrupt the inhibitory interaction between Beclin 1 and Bcl-2/Bcl-XL allowing Beclin 1 to maintain the class III phosphatidylinositol-3-kinase activity of Vps34 for the phagophore formation. Autophagy is a complex process that is regulated by multiple protein complexes beyond that organized around Beclin 1. The energy sensors including AMP-dependent kinase (AMPK), mammalian target of rapamycin (mTOR), Sirtuin1 (SIRT1) as well as stress-integrating pathways such as those involving the inhibitor of NF-κB (IκB) kinases (IKK) and the tumour suppressor protein p53, all have a major impact on the regulation of autophagy. In many paradigms of autophagic stimulation, they all seem to act upstream of the dissociation of Beclin 1-Bcl-2. Our results reveal that ABT737stimulate multiple pro-autophagic pathways to be optimally efficient. These results place SIRT1, AMPK/mTOR,HDM2 and IKK downstream of the dissociation of the Beclin 1-Bcl-2 complex. This study advocates that BH3mimetics trigger multiple autophagy-stimulatory pathways maybe due to the high degree of connectivity that exists among autophagy-regulatory protein complexes meaning that a specific effect on the Beclin 1-interactome might affect other nodes in the autophagy-controlling network. These pathways cannot follow a linear hierarchy and rather must be interconnected in a complex circuitry, in which stimulation of autophagy by physiological triggers (such as starvation or organelle stress) induce an ensemble of intimately linked changes that are coupled to each other in positive feed forward loops constituting an indissociable ensemble that composes the “autophagic switch”
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Petkova, Denitsa. "Étude du rôle de récepteurs autophagiques lors de l'infection par le virus de la rougeole." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10311/document.

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La macroautophagie assure l'homéostasie cellulaire en recyclant du matériel cytosolique obsolète ou délétère et sa dérégulation est associée à plusieurs pathologies. Elle constitue aussi un mécanisme de défense car elle peut éliminer des pathogènes intracellulaires. L'étape cruciale de l'autophagie est la maturation lors de laquelle la vésicule renfermant des substrats cytosoliques, l'autophagosome, fusionne avec des lysosomes et la dégradation a lieu. Nous nous intéressons à la régulation de l'autophagie et aux conséquences de sa perturbation lors des infections, notamment par le virus de la rougeole (VR). Les données de l'équipe montrent qu'il induit et utilise toutes les étapes de l'autophagie, afin de se répliquer efficacement. Mes travaux montrent que des protéines du virus peuvent interagir avec au moins deux protéines cellulaires NDP52 et T6BP qui sont des récepteurs autophagiques (protéines cytosoliques ayant un domaine de liaison aux autophagosomes et un domaine de liaison au substrat à dégrader, par exemple des pathogènes). J'ai alors étudié le rôle des récepteurs autophagiques T6BP, NDP52 et Optineurine dans la réplication virale. J'ai aussi participé à une étude décrivant que NDP52 et Optineurine régulent en plus la maturation. Mes travaux de thèse démontrent un tel double rôle pour T6BP. Cependant, seuls T6BP et NDP52 sont nécessaires à la réplication du VR bien qu'elle requiert la maturation autophagique. Ainsi mes résultats suggèrent d'une part que les trois récepteurs puissent réguler la maturation d'autophagosomes distincts.D'autre part, le VR pourrait exploiter individuellement les autophagosomes dont la maturation dépend de T6BP et NDP52 pour se répliquer
Macroautophagy ensures cell homeostasis through the recycling of obsolete or deleterious cytosolic components and its deregulation is associated with several pathologies. It is also a defense mechanism as it allows the elimination of intracellular pathogens. The most important autophagic step is maturation, during which the cytosolic substrate-containing vesicle, the autophagosome, fuses with lysosomes and the degradation occurs. We study autophagy regulation and the consequences of its disruption during infections and in particular by measles virus (MeV). Our team has shown that MeV induces and exploits all steps of autophagy, to replicate more efficiently. My results indicate that viral proteins can interact with at least two cellular proteins, NDP52 and T6BP, which are autophagy receptors (cytosolic proteins that carry an autophagosome-binding domain and a domain binding substrates that would be degraded, such as intracellular pathogens). I then studied the role of autophagic receptors T6BP, NDP52 and OPTINEURIN in viral replication. I also took part in a study describing NDP52 and OPTINEURIN as autophagosome maturation regulators. My work depicts the same dual role for T6BP. However, only T6BP and NDP52 are necessary for MeV replication even though it requires autophagosome maturation. Thus, my results suggest that the three autophagy receptors might regulate distinct autophagosome maturation on one hand. On the other, MeV could individually exploit autophagosomes, the maturation of which is regulated by T6BP or NDP2 to replicate efficiently
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Runwal, Gautam. "The study of two transmembrane autophagy proteins and the autophagy receptor, p62." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/290149.

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Autophagy is an evolutionarily conserved process across eukaryotes that is responsible for degradation of cargo such as aggregate-prone proteins, pathogens, damaged organelles, macromolecules etc. via its delivery to lysosomes. The process is known to involve the formation of a double-membraned structure, called autophagosome, that engulfs the cargo destined for degradation and delivers its contents by fusing with lysosomes. This process involves several proteins at its core which include two transmembrane proteins, ATG9 and VMP1. While ATG9 and VMP1 has been discovered for about a decade and half, the trafficking and function of these proteins remain relatively unclear. My work in this thesis identifies and characterises a novel trafficking route for ATG9 and VMP1 and shows that both these proteins traffic via the dynamin-independent ARF6-associated pathway. Moreover, I also show that these proteins physically interact with each other. In addition, the tools developed during these studies helped me identify a new role for the most common autophagy receptor protein, p62. I show that p62 can specifically associate with and sequester LC3-I in autophagy-impaired cells (ATG9 and ATG16 null cells) leading to formation of LC3-positive structures that can be misinterpreted as mature autophagosomes. Perturbations in the levels of p62 were seen to affect the formation of these LC3-positive structures in cells. This observation, therefore, questions the reliability of LC3-immunofluorescence assays in autophagy-impaired cells as method of assessing autophagy and points towards the homeostatic function played by p62 in autophagy-impaired cells.
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Scrivo, Aurora. "Régulation de la voie autophagique par la Gigaxonine E3-ligase, et implication dans les maladies neurodégénératives." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT090.

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L'autophagie est l'une des voies de signalisation qui maintiennent l'homéostasie cellulaire en condition basale, mais aussi en réponse à un stress. Son rôle est essentiel pour assurer plusieurs fonctions physiologiques, et son altération est associée à de nombreuses maladies, parmi lesquelles le cancer, les maladies immunitaires et les maladies neurodégénératives. Un nombre croissant d'études a établi que la voie autophagique est finement contrôlée. Cependant, très peu est connu sur les mécanismes moléculaires assurant sa régulation mais la famille des E3-ligases joue un rôle primordiale. La Gigaxonine est un adaptateur de la famille des E3 ligases CUL3, qui spécifie les substrats pour leur ubiquitination et leur successive dégradation. Des mutations «perte de fonction» de la Gigaxonine causent la Neuropathie à Axones Géants (NAG), une maladie neurodégénérative sévère et fatale, qui impacte tout le système nerveux et provoque une agrégation anormale des Filaments Intermédiaires (FI) dans l'organisme entier. Grâce à la modélisation de la pathologie dans les cellules de patients et chez la souris, le laboratoire a pu mettre en avant le rôle crucial de la Gigaxonine dans la dégradation de la famille des FIs, à travers son activité d'ubiquitination.Au cours de ma thèse, j'ai étudié les mécanismes de neurodégénerescence de la NAG, et la possible altération de la voie autophagique.Pour cela, j'ai développé un nouveau modèle neuronal de la maladie, à partir de notre modèle murin NAG, qui reproduit la mort neuronale et l'agrégation des FIs retrouvées chez les patients. Pour étudier l'implication de l'autophagie dans la neurodégénérescence, j'ai évalué l'effet de la déplétion de la Gigaxonine sur la formation des autophagosomes, le flux autophagique, la fusion avec le lysosome et la dégradation. J’ai ainsi révélé un défaut dans la dynamique autophagique dans les neurones NAG -/-. Pour déchiffrer les mécanismes moléculaires sous-jacents, j'ai étudié l'effet de l'absence de la Gigaxonine sur différentes régulateurs de la voie. En utilisant des techniques complémentaires, j'ai montré que la Gigaxonine est essentielle pour le turn-over d’un interrupteur autophagique, à travers son activité d’E3-ligase.En conclusion, nous avons identifié un nouveau mécanisme moléculaire impliqué dans le contrôle des premières phases de l'autophagie. Non seulement ces résultats présentent une avancée significative dans le domaine de l'autophagie, ils contribuent également à la compréhension de son dysfonctionnement dans les maladies neurodégénératives, et pourraient générer une nouvelle cible pour une intervention thérapeutique chez l'homme
The autophagic route is one of the signaling pathways that sustain cellular homeostasis in basal condition, but also in response to stress. It has been shown to be crucial for several physiological functions and its impairment is associated with many diseases, including cancer, immune and neurodegenerative diseases. While an expanding number of studies have shown that autophagic route is finely controlled, little is known about the molecular mechanisms ensuring its function, but a fundamental role is sustained by the family of E3 ligases. Gigaxonin is an adaptor of a Cul3-E3 ligase, which specifies the substrates for their ubiquitination and their subsequent degradation. “Loss of function” mutations in Gigaxonin cause Giant Axonal Neuropathy (GAN), a severe and fatal neurodegenerative disorder that impacts broadly the nervous system and cause an abnormal aggregation of Intermediate Filaments (IFs) through the body. Modeling the disease in patient’s cells and in mouse, the laboratory has demonstrated the crucial role of Gigaxonin in degrading the entire family of IFs through its ubiquitination activity.During my PhD, I studied the neurodegenerative mechanisms in GAN disease, and the possible impairment of autophagy pathway.For that purpose, I developed a new neuronal model of the disease from our GAN mouse, which reproduced the neurodegeneration and the IF aggregation found in patients. To investigate the involvement of autophagy in neurodegeneration, I evaluated the effect of Gigaxonin depletion on autophagosome formation, autophagic flux, lysosome fusion and degradation, and I revealed a defect in autophagy dynamics. To decipher the molecular mechanism of autophagosome impairment, I investigated the effect of Gigaxonin depletion on different autophagy regulators. Using complementary techniques, I showed that Gigaxonin is essential for the turn-over of a specific molecular switch, through its E3 ligase activity.Altogether, we identified a new exciting molecular mechanism in the control of autophagy. Not only these findings present a significant advance in the comprehension of the fundamental field of autophagy, but it also contribute in the understanding of its dysfunction in neurodegenerative diseases, and may generate a new target for therapeutic intervention in humans
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Osman, Ayman. "Autophagy in Peripheral Neuropathy." Doctoral thesis, Linköpings universitet, Avdelning för neurobiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-142125.

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Peripheral neuropathy includes a wide range of diseases affecting millions around the world, and many of these diseases have unknown etiology. Peripheral neuropathy in diabetes represents a large proportion of peripheral neuropathies. Nerve damage can also be caused by trauma. Peripheral neuropathies are a significant clinical problem and efficient treatments are largely lacking. In the case of a transected nerve, different methods have been used to repair or reconstruct the nerve, including the use of nerve conduits, but functional recovery is usually poor. Autophagy, a cellular mechanism that recycles damaged proteins, is impaired in the brain in many neurodegenerative diseases affecting animals and humans. No research, however, has investigated the presence of autophagy in the human peripheral nervous system. In this study, I present the first structural evidence of autophagy in human peripheral nerves. I also show that the density of autophagy structures is higher in peripheral nerves of patients with chronic idiopathic axonal polyneuropathy (CIAP) and inflammatory neuropathy than in controls. The density of these structures increases with the severity of the neuropathy. In animal model, using Goto-Kakizaki (GK) rats with diabetes resembling human type 2 diabetes, activation of autophagy by local administration of rapamycin incorporated in collagen conduits that were used for reconnection of the transected sciatic nerve led to an increase in autophagy proteins LC3 and a decrease in p62 suggesting that the autophagic flux was activated. In addition, immunoreactivity of neurofilaments, which are parts of the cytoskeleton of axons, was increased indicating increased axonal regeneration. I also show that many proteins involved in axonal regeneration and cell survival were up-regulated by rapamycin in the injured sciatic nerve of GK rats four weeks after injury. Taken together, these findings provide new knowledge about the involvement of autophagy in neuropathy and after peripheral nerve injury and reconstruction using collagen conduits.
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Yassine, Maya. "Calcium, Calcium-permeable channels and autophagy modulators in control of autophagy and cancer." Thesis, Lille 1, 2013. http://www.theses.fr/2013LIL10159/document.

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L'autophagie est une voie cellulaire strictement régulée dont le but principal est la dégradation lysosomale et le recyclage ultérieur du matériel cytoplasmique afin de maintenir l'homéostasie cellulaire normale. Des défauts dans l'autophagie sont liés à une variété d'états pathologiques, dont le cancer. Le cancer est une maladie associée aux modifications des processus cellulaires fondamentaux tels que l'apoptose et l'autophagie. Le calcium régule une série de processus physiologiques et pathologiques tels que le vieillissement, la neurodégénérescence et le cancer. Si le rôle du calcium et des canaux calciques dans le cancer est bien établi, l'information sur la nature moléculaire des canaux régulant l’autophagie ainsi que les mécanismes de cette régulation reste encore limitée. Le rôle de l'autophagie dans le cancer est complexe. En effet, elle peut favoriser à la fois la prévention tumorale et la résistance aux traitements. Elle est souvent détectée dans les cellules cancéreuses en réponse aux expositions aux rayons et la chimiothérapie. Elle semble contribuer à la résistance thérapeutique de certains cancers. Il est maintenant bien établi que sa modulation peut potentiellement contribuer à la mise en œuvre des méthodes de traitement du cancer. Dans cette étude, nos travaux ont permis d’identifier le calcium intracellulaire, comme un régulateur important de l'autophagie. Ainsi, nous proposons un lien possible entre le calcium, les canaux calciques, l’autophagie et la progression du cancer. De plus, nous avons mis en évidence un nouveau modulateur de l’autophagie, le ML-9. Cet outil pourrait cibler l'autophagie et être utilise dans le traitement des cancers
Autophagy is a tightly regulated cellular pathway the main purpose of which islysosomal degradation and subsequent recycling of cytoplasmic material to maintain normal cellular homeostasis. Defects in autophagy are linked to a variety of pathological states,including cancer. Cancer is the disease associated with abnormal tissue growth following an alteration in such fundamental cellular processes as apoptosis, proliferation, differentiation,migration and autophagy. Calcium is a ubiquitous secondary messenger which regulates plethora of physiological and pathological processes such as aging, neurodegeneration and cancer. The role of calcium and calcium-permeable channels in cancer is well-established, whereas theinformation about molecular nature of channels regulating autophagy and the mechanisms of this regulation is still limited. The role of autophagy in cancer is complex, as it can promoteboth tumor prevention and survival/treatment resistance. Elevated autophagy is often detected in cancer cells in response to radiation and chemotherapy. Furthermore, autophagy seems to contribute to the therapeutic resistance of some cancers. It's now clear that modulation of autophagy has a great potential in cancer diagnosis and treatment. Our findings identified intracellular calcium as an important regulator of autophagy. We propose a possible link between calcium, calcium permeable ion channels, autopohagy and cancer progression. Further, our results revealed a new autophagy modulator ML-9 as an attractive tool for targeting autophagy in cancer therapy
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McKnight, N. C. "A genome-wide screen for starvation-induced autophagy : identifies new modulators of autophagy." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1302281/.

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Autophagy is a catabolic mechanism by which cytoplasmic components are sequestered and transported by a double-membrane vesicle called an autophagosome to the lysosome for degradation. This recycling of organelles and macromolecules provides the cell with amino acids in times of nutrient deprivation though we do not fully know how the process is triggered or controlled. It is a highly regulated process in mammalian cells and its deregulation has been shown to contribute to multiple diseases. In order to find new regulators of mammalian autophagy, I performed a genome-wide screen using the Dharmacon human siRNA library in a stable human cell line expressing GFP-LC3, a specific marker for autophagosomal membranes. First I incubated the cells with the siRNA pools then I starved the cells of amino acids. This initiated the formation of GFP-LC3-labelled autophagosomes that I quantified using the Cellomics VTiScan microscope and accompanying software. I measured the effect of specific siRNA-mediated knock-down on multiple parameters including spot count. Accounting for cell death and normalising the data, I generated a Z-score for each siRNA pool and retested the best 500 autophagy-increasing and 500 autophagydecreasing siRNAs as above. The 190 strongest siRNA pools were deconvoluted leaving 20 hits that reproduced the phenotype with three or four out of four duplexes. These 20 hits were then assayed for endogenous LC3 lipidation in a different cell line and the ability of their siRNA to reduce mRNA levels was determined. Four increasers of GFP-LC3 spots increased endogenous LC3 lipidation, suggesting that these proteins are either negative regulators of autophagy or inhibit the maturation or degradation of autophagosomes. Five decreasers of GFP-LC3 spots also inhibited endogenous LC3 lipidation and I have characterised two of these proteins required for autophagy. SCOC colocalises with early autophagy markers and may be providing a scaffold for autophagy machinery. WAC, through its reported binding partners, may be playing a role in both the autophagic and ubiquitin/proteasome pathways.
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Otten, Elsje Gesina. "Molecular mechanisms of autophagy and the effect of autophagy dysfunction on mitochondrial function." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3953.

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Long lifespan of evolutionary higher organisms including humans is associated with the challenge to maintain viability of post mitotic cells, such as neurons, for decades. Autophagy is increasingly recognized as an important prosurvival pathway in oxidative and proteotoxic stress conditions. Autophagy degrades cytosolic macromolecules in response to starvation and is involved in the selective degradation of damaged/toxic organelles, such as mitochondria. With age autophagy function declines, and is also compromised in several neurodegenerative diseases. We identified a novel role for autophagy in the maintenance of mitochondrial health, specifically respiratory complex I. Intriguingly, galactose-induced cell death of autophagy deficient cells was rescued by preventing ROS production at complex I or bypassing complex I-linked respiration. We propose that aberrant ROS production via complex I in response to autophagy deficiency could be pathogenic and result in neurodegeneration and preventing this could be an interesting therapeutic target. Furthermore, we found that vertebrates have evolved mechanisms to induce autophagy in response to oxidative stress. This involves the oxidation of the autophagy receptor p62, which promotes autophagy flux and the clearance of autophagy cargo, resulting in increased stress resistance in mammalian cells and survival under stress in flies. In addition, we obtained data revealing an important role for redox-regulated cysteines in NDP52 for the degradation of mitochondria via mitophagy and tools were created to study the role of other autophagy receptors in autophagy initiation and selective autophagy.
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Books on the topic "Autophagy"

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Ktistakis, Nicholas, and Oliver Florey, eds. Autophagy. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0.

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Vojo, Deretic, ed. Autophagosome and phagosome / edited by Vojo Deretic. Totowa, NJ: Humana Press, 2008.

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Norberg, Helin, and Erik Norberg, eds. Autophagy and Cancer. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2071-7.

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Wang, Hong-Gang, ed. Autophagy and Cancer. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6561-4.

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Autophagy in infection and immunity. Dordrecht: Springer, 2009.

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Xie, Zhiping, ed. Autophagy: Biology and Diseases. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-2830-6.

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Qin, Zheng-Hong, ed. Autophagy: Biology and Diseases. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0602-4.

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Maiuri, Maria Chiara, and Daniela De Stefano, eds. Autophagy Networks in Inflammation. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30079-5.

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Le, Weidong, ed. Autophagy: Biology and Diseases. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-4272-5.

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service), ScienceDirect (Online, ed. Autophagy in mammalian systems. San Diego, Calif: Academic, 2009.

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Book chapters on the topic "Autophagy"

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Mortimore, Glenn E., Giovanni Miotto, Rina Venerando, and Motoni Kadowaki. "Autophagy." In Subcellular Biochemistry, 93–135. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5833-0_4.

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Zhang, Hao, Bilon Khambu, and Xiao-Ming Yin. "Autophagy." In Signaling Pathways in Liver Diseases, 151–65. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118663387.ch11.

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Tsugawa, Hitoshi, and Hidekazu Suzuki. "Autophagy." In Helicobacter pylori, 67–71. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55705-0_5.

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Rojas, Mollie K., Juel Chowdhury, Khatja Batool, Zane Deliu, and Abdallah Oweidi. "Autophagy." In Apoptosis and Beyond, 71–82. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119432463.ch4.

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Schalk, Amanda, and Sven Thoms. "Autophagy." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_487-3.

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Mehlhorn, Heinz. "Autophagy." In Encyclopedia of Parasitology, 245. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3666.

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Escobar, María Luisa, Gerardo H. Vázquez-Nin, and Olga M. Echeverría. "Autophagy." In Cell Death in Mammalian Ovary, 81–102. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1134-1_5.

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Mehlhorn, Heinz. "Autophagy." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3666-1.

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, Istvan Berczi, Kameljit Kalsi, José González-Alonso, David J. Dyck, et al. "Autophagy." In Encyclopedia of Exercise Medicine in Health and Disease, 112. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2129.

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Schalk, Amanda, and Sven Thoms. "Autophagy." In Encyclopedia of Cancer, 411–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_487.

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Conference papers on the topic "Autophagy"

1

Belyaeva, E. D., and D. R. Fayzullina. "CYTOMEGALOVIRUS MICRORNAS INHIBIT AUTOPHAGY." In OpenBio-2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-231.

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Cytomegalovirus persistence correlates with the aggressiveness of some human cancers. We have shown that the viral microRNA UL70-3P suppresses autophagy in glioblastoma cells. Regulatory molecules both act constitutively and are secreted as part of exosomes to influence the cell microenvironment.
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Bezrukova, A. I., K. S. Basharova, I. V. Miliukhina, S. N. Pchelina, and T. S. Usenko. "EXPRESSION OF AUTOPHAGY-RELATED GENES IN GBA1 MUTATIONS CARRIERS WITH AND WITHOUT PARKINSON’S DISEASE." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-297.

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The molecular mechanisms of the neurodegenerative disease, Parkinson’s disease (PD), associated with mutations in the GBA1 gene (GBA-PD) are unknown. Recent data point to the role of autophagy, in particular of the PI3K/AKT/mTOR pathway, in PD pathogenesis. The study revealed pronounced alterations in the expression of autophagy-related genes are involved in the PI3K/AKT/mTOR pathway in GBA-PD. v
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Goehe, Rachel W., Xu Di, Khushboo Sharma, Molly L. Bristol, Scott C. Henderson, Francis Rodier, Albert R. Davalos, and David A. Gewirtz. "Abstract 4652: The autophagy-senescence connection in chemotherapy of breast tumor cells; senescence accelerated by autophagy but not dependent on autophagy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4652.

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Cabrera, S., C. Rodriguez-Bobadilla, M. Gaxiola, D. Vazquez-Morales, M. Selman, and A. Pardo. "Autophagy Biomarkers in Hypersensitivity Pneumonitis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5559.

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Yang, Sei-Hoon, Kang Kyoo Lee, and Sun Rock Moon. "Abstract 2271: Autophagy induction by low dose cisplatin: The role of p53 in autophagy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2271.

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Nehme, Grace, Kumar Felix, Andrew Wahba, Diana M. Fandino, and Nancy Gordon. "Abstract A03: Autophagy and HSP27: A potential link to define autophagy fate in osteosarcoma." In Abstracts: AACR Special Conference on Targeting PI3K/mTOR Signaling; November 30-December 8, 2018; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.pi3k-mtor18-a03.

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Pulido, Ines, Juan L. Pascual, Margaret Soucheray, Maria L. Rodriguez, Daniel T. Crespo, Salvador Aparisi, Joan A. Sirerol, et al. "Abstract 753: Genomic alterations of autophagy genes disrupts autophagic flux in human lung adenocarcinomas." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-753.

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Lorenzo, Irene, Jose Antonio Pinto Tasende, Natividad Oreiro, Francisco J. Blanco, and Beatriz Carames. "FRI0515 HSP90AA1, A CHAPERONE-MEDIATED AUTOPHAGY, IS A BIOMARKER ASSOCIATED WITH DEFECTIVE AUTOPHAGY IN OSTEOARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4839.

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Gump, Jacob M. "Abstract 86: Role of autophagy in lymphoma treatment: Autophagy manipulation in lymphoma therapeutic cell killing." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-86.

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Liu, Xiao-Ling. "DECIPHERING THE GENETIC LINKS BETWEEN PSYCHOLOGICAL STRESS, AUTOPHAGY, AND DERMATOLOGICAL HEALTH: INSIGHTS FROM BIOINFORMATICS, SINGLE-CELL ANALYSIS, AND MACHINE LEARNING IN PSORIASIS AND ANXIETY DISORDERS." In BioClina 2024 – International Conference on Biological & Clinical Studies, 21-22 June, Singapore. Global Research & Development Services, 2024. http://dx.doi.org/10.20319/icrlsh.2024.8687.

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The relationship between psychological stress, altered skin immunity, and autophagy-related genes (ATGs) is currently unclear. Psoriasis is a chronic skin inflammation of unclear etiology that is characterized by persistence and recurrence. Immune dysregulation and emotional disturbances are recognized as significant risk factors. Emerging clinical evidence suggests a possible connection between anxiety disorders, heightened immune system activation, and altered skin immunity, offering a fresh perspective on the initiation of psoriasis. The aim of this study was to explore the potential shared biological mechanisms underlying the comorbidity of psoriasis and anxiety disorders. Psoriasis and anxiety disorders data were obtained from the GEO database. A list of 3254 ATGs was obtained from the public database. Differentially expressed genes (DEGs) were obtained by taking the intersection of DEGs between psoriasis and anxiety disorder samples and the list of ATGs. Five machine learning algorithms used screening hub genes. The ROC curve was performed to evaluate diagnostic performance. Then, GSEA, immune infiltration analysis, and network analysis were carried out. The Seurat and Monocle algorithms were used to depict T-cell evolution. Cellchat was used to infer the signaling pathway between keratinocytes and immune cells. Four key hub genes were identified as diagnostic genes related to psoriasis autophagy. Enrichment analysis showed that these genes are indeed related to T cells, autophagy, and immune regulation, and have good diagnostic efficacy validated. Using single-cell RNA sequencing analysis, we expanded our understanding of key cellular participants, including inflammatory keratinocytes and their interactions with immune cells. We found that the CASP7 gene is involved in the T-cell development process, and correlated with γδ T cells, warranting further investigation. We found that anxiety disorders are related to increased autophagy regulation, immune dysregulation, and inflammatory response, and are reflected in the onset and exacerbation of skin inflammation. The hub gene is involved in the process of immune signaling and immune regulation. The CASP7 gene, which is related with the development and differentiation of T cells, deserves further study. Potential biomarkers between psoriasis and anxiety disorders were identified, which are expected to aid in the prediction of disease diagnosis and the development of personalized treatments.
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Reports on the topic "Autophagy"

1

Eastman, Alan. Improved Therapy for Breast Cancer by Inhibiting Autophagy. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada514577.

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Keating, Amy. Targeting Pediatric Glioma with Apoptosis and Autophagy Manipulation. Fort Belvoir, VA: Defense Technical Information Center, August 2012. http://dx.doi.org/10.21236/ada567861.

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3

Lock, Rebecca. Detachment-Induced Autophagy and Breast Cancer Cell Survival. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada559641.

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Keating, Amy. Targeting Pediatric Glioma with Apoptosis and Autophagy Manipulation. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada614915.

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5

Kongara, Sameera. Role of Autophagy in Keratin Homeostasis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2012. http://dx.doi.org/10.21236/ada583662.

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Kongara, Sameera. Role of Autophagy in Keratin Homeostasis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2014. http://dx.doi.org/10.21236/ada601249.

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7

Evans, Christopher P. Overcoming Autophagy to Induce Apoptosis in Castration-Resistant Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613417.

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8

Yang, Jin-Ming. The Importance of Autophagy in Breast Cancer Development and Treatment. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada542209.

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Yang, Jin-Ming. The Importance of Autophagy in Breast Cancer Development and Treatment. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada516336.

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Yang, Jin-Ming. The Importance of Autophagy in Breast Cancer Development and Treatment. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada525625.

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