Bibliografie tematiche / Lipophagie

Letteratura scientifica selezionata sul tema "Lipophagie"

Autore: Grafiati

Pubblicato: 22 giugno 2024

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Articoli di riviste sul tema "Lipophagie":

Zelickson, B. D., e R. K. Winkelmann. "Lipophagic panniculitis in re-excision specimens." Acta Dermato-Venereologica 71, n. 1 (1 gennaio 1991): 59–61. http://dx.doi.org/10.2340/00015555715961.

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Lipophagic panniculitis consists of a macrophage infiltrate in the subcutaneous tissue. The macrophages transform into foam cells within the panniculus they replace lipocytes and may form giant cells. Although those pathologic features have been described as diagnostic of Weber-Christian disease, we report the occurrence of lipophagic panniculitis in re-excision specimens. Among 252 re-excision specimens from previously biopsied skin tumors, 5 cases in which masses of lipophages were infiltrating and replacing the subcutaneous tissue were found. The infiltrate was localized to the deep dermis and superficial subcutaneous tissue below and beside the initial biopsy site. In 3 cases, suture or hair was detected within the tissue, and granulation tissue with foreign body giant cells was observed along the dermal suture line. In 4 cases there was evidence of phlebitis within or close to areas of infiltration. None of these patients developed symptomatic panniculitis. Lipophagia can be a normal response of wound healing in some patients.

Schott, Micah B., Shaun G. Weller, Ryan J. Schulze, Eugene W. Krueger, Kristina Drizyte-Miller, Carol A. Casey e Mark A. McNiven. "Lipid droplet size directs lipolysis and lipophagy catabolism in hepatocytes". Journal of Cell Biology 218, n. 10 (7 agosto 2019): 3320–35. http://dx.doi.org/10.1083/jcb.201803153.

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Lipid droplet (LD) catabolism in hepatocytes is mediated by a combination of lipolysis and a selective autophagic mechanism called lipophagy, but the relative contributions of these seemingly distinct pathways remain unclear. We find that inhibition of lipolysis, lipophagy, or both resulted in similar overall LD content but dramatic differences in LD morphology. Inhibition of the lipolysis enzyme adipose triglyceride lipase (ATGL) resulted in large cytoplasmic LDs, whereas lysosomal inhibition caused the accumulation of numerous small LDs within the cytoplasm and degradative acidic vesicles. Combined inhibition of ATGL and LAL resulted in large LDs, suggesting that lipolysis targets these LDs upstream of lipophagy. Consistent with this, ATGL was enriched in larger-sized LDs, whereas lipophagic vesicles were restricted to small LDs as revealed by immunofluorescence, electron microscopy, and Western blot of size-separated LDs. These findings provide new evidence indicating a synergistic relationship whereby lipolysis targets larger-sized LDs to produce both size-reduced and nascently synthesized small LDs that are amenable for lipophagic internalization.

Jonas, Wenke, Kristin Schwerbel, Lisa Zellner, Markus Jähnert, Pascal Gottmann e Annette Schürmann. "Alterations of Lipid Profile in Livers with Impaired Lipophagy". International Journal of Molecular Sciences 23, n. 19 (6 ottobre 2022): 11863. http://dx.doi.org/10.3390/ijms231911863.

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Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Various mechanisms such as an increased uptake in fatty acids or de novo synthesis contribute to the development of steatosis and progression to more severe stages. Furthermore, it has been shown that impaired lipophagy, the degradation of lipids by autophagic processes, contributes to NAFLD. Through an unbiased lipidome analysis of mouse livers in a genetic model of impaired lipophagy, we aimed to determine the resulting alterations in the lipidome. Observed changes overlap with those of the human disease. Overall, the entire lipid content and in particular the triacylglycerol concentration increased under conditions of impaired lipophagy. In addition, we detected a reduction in long-chain polyunsaturated fatty acids (PUFAs) and an increased ratio of n-6 PUFAs to n-3 PUFAs, which was due to the depletion of n-3 PUFAs. Although the abundance of major phospholipid classes was reduced, the ratio of phosphatidylcholines to phosphatidylethanolamines was not affected. In conclusion, this study demonstrates that impaired lipophagy contributes to the pathology of NAFLD and is associated with an altered lipid profile. However, the lipid pattern does not appear to be specific for lipophagic alterations, as it resembles mainly that described in relation to fatty liver disease.

Alexandrides, C. "Lipophagic Granuloma". Acta Medica Scandinavica 154, S312 (24 aprile 2009): 449–60. http://dx.doi.org/10.1111/j.0954-6820.1956.tb17036.x.

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Peng, Peng, Wensheng Liu, Adam Utley, Colin Chavel, Louise Carlson, Scott H. Olejniczak e Kelvin P. Lee. "CD28 Induces Autophagy in Plasma Cells to Enhance Mitochondrial Respiration and Survival". Journal of Immunology 204, n. 1_Supplement (1 maggio 2020): 71.2. http://dx.doi.org/10.4049/jimmunol.204.supp.71.2.

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Abstract Durable humoral immunity relies on the persistence of long-lived plasma cells (LLPC) that continuously produce protective antibodies. The prototypical T cell costimulatory molecule CD28, that is also expressed on LLPC, is critical to their survival but the mechanisms involved remain unclear. We found CD28 activation enhances autophagy in LLPC/multiple myeloma as evidenced by increased level of autophagy marker LC3II, elevated autophagosome numbers and decreased level of autophagic cargo receptor P62. Inhibition of autophagy by 3MA or BafA abolished CD28’s pro-survival effects. Mechanistically, CD28 activation increased the protein level of ATG5, a critical autophagy regulator, even with translation blockade, but this was abrogated by proteasome inhibition. Knocking down atg5 eliminated CD28’s pro-survival effects, suggesting CD28 signaling regulates ATG5 degradation to sustain pro-survival autophagy. CD28 activation significantly increased mitochondrial respiration and blocking autophagy prevented this. Free fatty acids (FFA) can be degraded from cellular lipid droplets (LD) by lipophage, a selective form of autophagy, to fuel mitochondrial respiration. We found CD28 activation decreased LD staining and blocking autophagy prevented this. Blocking lipophagic lipase by lalistat eliminated CD28-induced oxidative phosphorylation and pro-survival effects. Addition of FFA (oleic and palmitic acids) boosted oxidative phosphorylation and restored survival with autophagy inhibition but not with fatty acid oxidation blockade. These data suggest CD28 signaling regulates ATG5 protein degradation to enhance autophagy and this in return produces FFA to sustain mitochondrial respiration and support LLPC survival.

Kumar, Ravinder, Muhammad Arifur Rahman e Taras Y. Nazarko. "Nitrogen Starvation and Stationary Phase Lipophagy Have Distinct Molecular Mechanisms". International Journal of Molecular Sciences 21, n. 23 (29 novembre 2020): 9094. http://dx.doi.org/10.3390/ijms21239094.

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In yeast, the selective autophagy of intracellular lipid droplets (LDs) or lipophagy can be induced by either nitrogen (N) starvation or carbon limitation (e.g., in the stationary (S) phase). We developed the yeast, Komagataella phaffii (formerly Pichia pastoris), as a new lipophagy model and compared the N-starvation and S-phase lipophagy in over 30 autophagy-related mutants using the Erg6-GFP processing assay. Surprisingly, two lipophagy pathways had hardly overlapping stringent molecular requirements. While the N-starvation lipophagy strictly depended on the core autophagic machinery (Atg1-Atg9, Atg18, and Vps15), vacuole fusion machinery (Vam7 and Ypt7), and vacuolar proteolysis (proteinases A and B), only Atg6 and proteinases A and B were essential for the S-phase lipophagy. The rest of the proteins were only partially required in the S-phase. Moreover, we isolated the prl1 (for the positive regulator of lipophagy 1) mutant affected in the S-phase lipophagy, but not N-starvation lipophagy. The prl1 defect was at a stage of delivery of the LDs from the cytoplasm to the vacuole, further supporting the mechanistically different nature of the two lipophagy pathways. Taken together, our results suggest that N-starvation and S-phase lipophagy have distinct molecular mechanisms.

Levy, Jack, Mark E. Burnett e Cynthia M. Magro. "Lipophagic Panniculitis of Childhood". American Journal of Dermatopathology 39, n. 3 (marzo 2017): 217–24. http://dx.doi.org/10.1097/dad.0000000000000721.

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UMBERT, I. J., e R. K. WINKELMANN. "Adult lipophagic atrophic panniculitis". British Journal of Dermatology 124, n. 3 (marzo 1991): 291–95. http://dx.doi.org/10.1111/j.1365-2133.1991.tb00578.x.

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Winkelmann, R. K., Marian T. McEvoy e Margot S. Peters. "Lipophagic panniculitis of childhood". Journal of the American Academy of Dermatology 21, n. 5 (novembre 1989): 971–78. http://dx.doi.org/10.1016/s0190-9622(89)70285-1.

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Juneja, Manish, Pankaj Raut, Milind Lohkare, Harshawardhan Ramteke, Vaishnavi Walke e Sakshi Bhatia. "Effects of Lipophagy on Atherosclerosis". Central India Journal of Medical Research 2, n. 01 (15 maggio 2023): 17–25. http://dx.doi.org/10.58999/cijmr.v2i01.44.

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Abstract (sommario):

An excess build-up of lipids in the arterial wall might result into Atherosclerosis. Lipophagy is the autophagic degradation of lipids that regulates the lipid metabolism in various kinds of cells. Lipophagy replaces intracellular lipid which makes it vital for development and progression of atherosclerosis. This review focuses on advances in lipid metabolism through lipophagy. The role of lipophagy in vascular endothelial cell injury, macrophage lipid accumulation and vascular smooth muscle cells phenotypic shift has been explained by specifying the lipophagy– atherosclerosis relationship. Novel therapeutic choices can be discovered by understanding the significance of lipophagy in these processes which could be a breakthrough in treatment of atherosclerosis.

Più fonti

Tesi sul tema "Lipophagie":

Chang, Yu-Chin, e 張毓秦. "Activation of lipophagy protects neurons from neurodegeneration caused by sphingolipid imbalance". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/59910094618794899139.

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碩士
國立臺灣大學
生理學研究所
104
Sphingolipids are essential membrane components of the neuron; hence their levels need to be tightly regulated. Infertile crescent (Ifc) is an evolutionarily conserved dihydroceramide (DHC) desaturase which converts DHC to Ceramide (Cer) for the de novo synthesis of Cer in Drosophila. While the imbalance of Cer, a bioactive sphingolipid, has been associated with several neurodegenerative diseases, the neuronal function of its precursor DHC remains unknown. To investigate the role of ifc, we generated ifc knockout flies (ifc-KO). Sphingolipidomic analysis showed that loss of ifc resulted in increased DHC. Prolonged light stimuli to the ifc-KO eye led to activity-dependent degeneration of photoreceptors. Clonal analysis of ifc-KO photoreceptors revealed the accumulation of lipophagic structure and the increased H2DCF signals upon light stimuli, suggesting that DHC accumulation may activate lipophagy and induce the production of reactive oxygen species (ROS). However, it remains to be determined whether the degeneration is attributed to lipophagic cell death or the ROS insults. Reduction of ifc led to the increase of Atg8/LC3 puncta in the acidified compartment and elevation of lysosomal proteases, indicating the activated lipophagy can promote subsequent lysosomal function. ifc-dependent neurodegeneration can be partially rescued by an antioxidant AD4, indicating that ROS is at least partially responsible for the degeneration. In addition, both ROS elevation and lipid accumulation in ifc-KO was suppressed by treating with the autophagy inducer Rapamycin, suggesting that enhanced lipophagy plays a protective role in ifc-dependent neurodegeneration. Conversely, lipophagy can be downregulated by AD4, indicating ROS insults lead to the feedback upregulation of protective lipophagy. In summary, loss of ifc results in DHC accumulation and ROS generation, the latter of which subsequently activates lipophagy to protect against neurodegeneration. These findings support our hypothesis that DHC is bio-active and lipophagy can be protective, highlighting their potential as therapeutic targets for regulating sphingolipid homeostasis.

Christian, Patricia. "Investigating the Role of Autophagy in Intracellular Apolipoprotein B Traffic and Very-low-density-lipoprotein Assembly and Secretion". Thesis, 2013. http://hdl.handle.net/1807/42743.

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Apolipoprotein B (apoB) is the main protein of very-low-density lipoprotein (VLDL). As apoB is translated and moves through the secretory pathway, lipids from cytoplasmic lipid droplets (LDs) are added to form VLDL particles. Without adequate lipid availability, apoB is misfolded and undergoes proteasomal degradation; however, evidence now shows that apoB can be degraded through autophagy. Inhibiting autophagy decreased apoB localization to autophagosomes in HepG2 cells, but also decreased apoB recovered from cells and media. Inducing autophagy increased apoB localization to autophagosomes and decreased apoB recovery. LDs are also degraded through autophagy however LDs were not affected by autophagy modulation in HepG2 cells. In primary hamster hepatocytes, inhibiting autophagy reduced apoB-autophagosome co-localization and increased LD numbers. These data suggest that autophagy may play a complex role in VLDL assembly by regulating degradation of both apoB and LDs. This dual role is more evident in primary hepatocytes indicating a potential physiological role.

Capitoli di libri sul tema "Lipophagie":

Martinez-Lopez, Nuria. "Regulation of Lipophagy". In Autophagy and Signaling, 147–72. Boca Raton, FL : CRC Press, 2018. | Series: Methods in signal transduction series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315120638-10.

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Steinberg, Christian E. W. "Lipid Homeostasis and Lipophagy—‘The Greasy Stuff Balanced’". In Aquatic Animal Nutrition, 583–97. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87227-4_24.

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Magro, Cynthia M., e Josh H. Mo. "Lipophagic/Lipoatrophic Panniculitis: A TH1-Mediated Autoimmune Disorder of the Subcutaneous Fat". In New and Emerging Entities in Dermatology and Dermatopathology, 277–86. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80027-7_21.

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Sathyanarayan, Aishwarya. "A Coupled Approach Utilizing Immunohistochemistry and Immunocytochemistry to Visualize Cellular Lipophagy". In Methods in Molecular Biology, 185–91. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6759-9_11.

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Sathyanarayan, Aishwarya. "Erratum to: A Coupled Approach Utilizing Immunohistochemistry and Immunocytochemistry to Visualize Cellular Lipophagy". In Methods in Molecular Biology, E1. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6759-9_21.

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"Lipophagic panniculitis of childhood". In Dermatology Therapy, 358. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1645.

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Cristobal-Sarramian, A., M. Radulovic e S. D. Kohlwein. "Methods to Measure Lipophagy in Yeast". In Methods in Enzymology, 395–412. Elsevier, 2017. http://dx.doi.org/10.1016/bs.mie.2016.09.087.

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Dutta, Shweta, Saraswati Prasad Mishra, Anil Kumar Sahu, Koushlesh Mishra, Pankaj Kashyap e Bhavna Sahu. "Hepatocytes and Its Role in Metabolism". In Drug Metabolism [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99083.

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Abstract (sommario):

Liver is one of the vital organ that performs many functions in the human body. Prominently it acts as a metabolizing organ for the body. This chapter elaborately describes hepatocytes along with their morphological features. In addition, it explains the structure of hepatocytes and different parts such as kupffer cells, hepatic stellate and hepatic sinusoids. Moreover present chapter elaborates the varieties of functions that hepatocytes perform such as filtration of blood, acting as a viral incubator, lipophagy and regulation of insulin and glucose. This chapter also explains hepatic injury that is caused by chronic consumption of alcohol along with the mechanism behind it.

Roccio, Federica, Aurore Claude-Taupin, Joëlle Botti, Etienne Morel, Patrice Codogno e Nicolas Dupont. "Monitoring lipophagy in kidney epithelial cells in response to shear stress". In Methods in Cell Biology. Elsevier, 2021. http://dx.doi.org/10.1016/bs.mcb.2020.12.003.

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Esmaeilian, Yashar, Sevgi Yusufoglu, Ece Iltumur, Gamze Bildik e Ozgur Oktem. "Visualizing Lipophagy as a New Mechanism of the Synthesis of Sex Steroids in Human Ovary and Testis Using Immunofluorescence Staining Method". In Methods in Molecular Biology. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/7651_2024_520.

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Atti di convegni sul tema "Lipophagie":

Irungbam, K., Y. Churin, M. Ocker, M. Roderfeld e E. Roeb. "CB1 knockout alleviates hepatic steatosis via lipophagy and lipolysis in HBs transgenic mice". In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677164.

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