Готові списки джерел за темами / Apoptose mitochondriale

Добірка наукової літератури з теми "Apoptose mitochondriale"

Автор: Grafiati
Опубліковано: 7 липня 2024

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Статті в журналах з теми "Apoptose mitochondriale":

1

Zweck, Elric, Julia Szendrödi, Malte Kelm, and Michael Roden. "Das diabetische Herz und Herzinsuffizienz – Aktuelles zu Entstehung und Therapie." DMW - Deutsche Medizinische Wochenschrift 144, no. 03 (January 31, 2019): 175–79. http://dx.doi.org/10.1055/a-0646-7871.

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Was ist neu? Klinisches Bild Typ-2-Diabetes-mellitus (T2 D) ist ein unabhängiger Risikofaktor für Herzinsuffizienz, die als Komplikation oftmals unterschätzt wird. Bei T2 D kann sich früh eine diastolische Funktionsstörung ausbilden, die sich später zu einer Herzinsuffizienz entwickeln kann. Von einer ischämischen Kardiomyopathie ist eine Diabetes-bedingte Herzinsuffizienz aktuell nicht abgrenzbar. Pathophysiologie Hyperglykämie, Hyperinsulinämie und Hyperlipidämie bei T2 D verändern den myokardialen Stoffwechsel. Daraus resultieren oxidativer Stress, reduzierte mitochondriale Effizienz, Lipotoxizität und Apoptose im Herzen. Die T2D-assoziierte nicht-alkoholische Fettlebererkrankung (NAFLD) zeigt ähnliche Pathomechanismen und stellt einen potenziellen Risikofaktor dar. Therapiestrategien Zur Verbesserung der Herzfunktion wird die Kontrolle kardiovaskulärer Risikofaktoren sowie Reduktion der Insulinresistenz durch Bewegung und Gewichtsabnahme empfohlen. Neben Metformin scheinen SGLT2-Inhibitoren als zusätzliche Therapieoption besonders geeignet zu sein. Auch die NAFLD könnte ein Angriffspunkt zukünftiger Therapieansätze werden.
2

Adhihetty, Peter J., Vladimir Ljubicic, and David A. Hood. "Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E748—E755. http://dx.doi.org/10.1152/ajpendo.00311.2006.

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Chronic contractile activity of skeletal muscle induces an increase in mitochondria located in proximity to the sarcolemma [subsarcolemmal (SS)] and in mitochondria interspersed between the myofibrils [intermyofibrillar (IMF)]. These are energetically favorable metabolic adaptations, but because mitochondria are also involved in apoptosis, we investigated the effect of chronic contractile activity on mitochondrially mediated apoptotic signaling in muscle. We hypothesized that chronic contractile activity would provide protection against mitochondrially mediated apoptosis despite an elevation in the expression of proapoptotic proteins. To induce mitochondrial biogenesis, we chronically stimulated (10 Hz; 3 h/day) rat muscle for 7 days. Chronic contractile activity did not alter the Bax/Bcl-2 ratio, an index of apoptotic susceptibility, and did not affect manganese superoxide dismutase levels. However, contractile activity increased antiapoptotic 70-kDa heat shock protein and apoptosis repressor with a caspase recruitment domain by 1.3- and 1.4-fold ( P < 0.05), respectively. Contractile activity elevated SS mitochondrial reactive oxygen species (ROS) production 1.4- and 1.9-fold ( P < 0.05) during states IV and III respiration, respectively, whereas IMF mitochondrial state IV ROS production was suppressed by 28% ( P < 0.05) and was unaffected during state III respiration. Following stimulation, exogenous ROS treatment produced less cytochrome c release (25–40%) from SS and IMF mitochondria, and also reduced apoptosis-inducing factor release (≈30%) from IMF mitochondria, despite higher inherent cytochrome c and apoptosis-inducing factor expression. Chronic contractile activity did not alter mitochondrial permeability transition pore (mtPTP) components in either subfraction. However, SS mitochondria exhibited a significant increase in the time to Vmax of mtPTP opening. Thus, chronic contractile activity induces predominantly antiapoptotic adaptations in both mitochondrial subfractions. Our data suggest the possibility that chronic contractile activity can exert a protective effect on mitochondrially mediated apoptosis in muscle.
3

Wissel, Kirsten, Elisabeth Berger, Gudrun Brandes, Gerrit Paasche, Thomas Lenarz, and Martin Durisin. "Erratum: Wie beeinflussen Platin-Nanopartikel die Zellviabilität der Corti-Organ Zelllinie der Maus (HEI-OC1) und der Spiralganglienzellen postnataler Ratten in Kultur?" Laryngo-Rhino-Otologie 101, S 02 (May 2022): e1-e2. http://dx.doi.org/10.1055/a-2004-8821.

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Einleitung Systemische Kortison- und Antibiotikagabe können bei einem geringen Prozentsatz der CI-Träger die erhöhten Impedanzen nicht normalisieren. In Studien werden erodierte Platinelektrodenkontakte als mögliche Ursache genannt. Ziel dieser Studie ist die Charakterisierung der Effekte von Platin-Nanopartikeln (Pt-NP, 3 nm) auf die HEI-OC1-Zellen und Spiralganglionneuronen (SGN) in der Zellkultur. Methoden Die metabolische Aktivität mittels Resazurin wurde in den HEI-OC1-Zellen mit 50–150 µg/ml Pt-NP ermittelt. Die Überlebensrate und das Neuritenwachstum der SGN, dissoziiert aus den postnatalen Ratten (P5) und kultiviert für 48 h, wurde nach Gabe der Pt-NP (20–100 µg/ml) mittels Färbung der Neurofilament-Antigene quantitativ bestimmt. Mittels Raster- (REM) und Transmissionselektronenmikroskopie (TEM) wurden Veränderungen der Morphologie und der Ultrastrukturen der Zellen analysiert. Ergebnisse Pt-NP zwischen 75 und 150 µg/ml reduzierten die metabolische Aktivität der HEI-OC1-Zellen, ohne jedoch zytotoxisch zu wirken. REM und TEM zeigten, dass 100 µg/ml Pt-NP nicht nur die Apoptose, sondern auch Reparaturvorgänge mitels des autophagosomal-lysosomalen Systems induzierten. Bei keiner Pt-NP-Konzentration wurde ein SGN-Verlust oder eine Reduktion des Neuritenwachstums gefunden. Schlußfolgerungen Pt-NP reduzierten in Konzentrationen ab 75 µg/ml die mitochondriale Aktivität in den HEI-OC1-Zellen, induzierten jedoch nicht den Zelltod. TEM weist dagegen auf effektive Reparaturmechanismen hin. Im Vergleich dazu führten Pt-NP zu keiner direkten Beeinträchtigung des SGN-Stoffwechsels. Es ist zu untersuchen, ob eine Exposition der SGN und Gliazellen mit PT-NP über eine längere Kultivierungsdauer zur Schädigung des Stoffwechsels der Neuronen führt.
4

Breckenridge, David G., Marina Stojanovic, Richard C. Marcellus, and Gordon C. Shore. "Caspase cleavage product of BAP31 induces mitochondrial fission through endoplasmic reticulum calcium signals, enhancing cytochrome c release to the cytosol." Journal of Cell Biology 160, no. 7 (March 31, 2003): 1115–27. http://dx.doi.org/10.1083/jcb.200212059.

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Stimulation of cell surface death receptors activates caspase-8, which targets a limited number of substrates including BAP31, an integral membrane protein of the endoplasmic reticulum (ER). Recently, we reported that a caspase-resistant BAP31 mutant inhibited several features of Fas-induced apoptosis, including the release of cytochrome c (cyt.c) from mitochondria (Nguyen, M., D.G. Breckenridge, A. Ducret, and G.C. Shore. 2000. Mol. Cell. Biol. 20:6731–6740), implicating ER-mitochondria crosstalk in this pathway. Here, we report that the p20 caspase cleavage fragment of BAP31 can direct pro-apoptotic signals between the ER and mitochondria. Adenoviral expression of p20 caused an early release of Ca2+ from the ER, concomitant uptake of Ca2+ into mitochondria, and mitochondrial recruitment of Drp1, a dynamin-related protein that mediates scission of the outer mitochondrial membrane, resulting in dramatic fragmentation and fission of the mitochondrial network. Inhibition of Drp1 or ER-mitochondrial Ca2+ signaling prevented p20-induced fission of mitochondria. p20 strongly sensitized mitochondria to caspase-8–induced cyt.c release, whereas prolonged expression of p20 on its own ultimately induced caspase activation and apoptosis through the mitochondrial apoptosome stress pathway. Therefore, caspase-8 cleavage of BAP31 at the ER stimulates Ca2+-dependent mitochondrial fission, enhancing the release of cyt.c in response to this initiator caspase.
5

Basu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed, and Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation." Journal of Biological Chemistry 295, no. 52 (October 30, 2020): 18406–25. http://dx.doi.org/10.1074/jbc.rev120.011202.

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Mitochondria are specialized compartments that produce requisite ATP to fuel cellular functions and serve as centers of metabolite processing, cellular signaling, and apoptosis. To accomplish these roles, mitochondria rely on the genetic information in their small genome (mitochondrial DNA) and the nucleus. A growing appreciation for mitochondria's role in a myriad of human diseases, including inherited genetic disorders, degenerative diseases, inflammation, and cancer, has fueled the study of biochemical mechanisms that control mitochondrial function. The mitochondrial transcriptional machinery is different from nuclear machinery. The in vitro re-constituted transcriptional complexes of Saccharomyces cerevisiae (yeast) and humans, aided with high-resolution structures and biochemical characterizations, have provided a deeper understanding of the mechanism and regulation of mitochondrial DNA transcription. In this review, we will discuss recent advances in the structure and mechanism of mitochondrial transcription initiation. We will follow up with recent discoveries and formative findings regarding the regulatory events that control mitochondrial DNA transcription, focusing on those involved in cross-talk between the mitochondria and nucleus.
6

Kokkinopoulou, Ioanna, and Paraskevi Moutsatsou. "Mitochondrial Glucocorticoid Receptors and Their Actions." International Journal of Molecular Sciences 22, no. 11 (June 3, 2021): 6054. http://dx.doi.org/10.3390/ijms22116054.

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Mitochondria are membrane organelles present in almost all eukaryotic cells. In addition to their well-known role in energy production, mitochondria regulate central cellular processes, including calcium homeostasis, Reactive Oxygen Species (ROS) generation, cell death, thermogenesis, and biosynthesis of lipids, nucleic acids, and steroid hormones. Glucocorticoids (GCs) regulate the mitochondrially encoded oxidative phosphorylation gene expression and mitochondrial energy metabolism. The identification of Glucocorticoid Response Elements (GREs) in mitochondrial sequences and the detection of Glucocorticoid Receptor (GR) in mitochondria of different cell types gave support to hypothesis that mitochondrial GR directly regulates mitochondrial gene expression. Numerous studies have revealed changes in mitochondrial gene expression alongside with GR import/export in mitochondria, confirming the direct effects of GCs on mitochondrial genome. Further evidence has made clear that mitochondrial GR is involved in mitochondrial function and apoptosis-mediated processes, through interacting or altering the distribution of Bcl2 family members. Even though its exact translocation mechanisms remain unknown, data have shown that GR chaperones (Hsp70/90, Bag-1, FKBP51), the anti-apoptotic protein Bcl-2, the HDAC6- mediated deacetylation and the outer mitochondrial translocation complexes (Tom complexes) co-ordinate GR mitochondrial trafficking. A role of mitochondrial GR in stress and depression as well as in lung and hepatic inflammation has also been demonstrated.
7

Kim, Sin Ri, Ji Won Park, You-Jin Choi, Seong Keun Sonn, Goo Taeg Oh, Byung-Hoon Lee, and Tong-Shin Chang. "Mitochondrial H2O2 Is a Central Mediator of Diclofenac-Induced Hepatocellular Injury." Antioxidants 13, no. 1 (December 21, 2023): 17. http://dx.doi.org/10.3390/antiox13010017.

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Nonsteroidal anti-inflammatory drug (NSAID) use is associated with adverse consequences, including hepatic injury. The detrimental hepatotoxicity of diclofenac, a widely used NSAID, is primarily connected to oxidative damage in mitochondria, which are the primary source of reactive oxygen species (ROS). The primary ROS responsible for inducing diclofenac-related hepatocellular toxicity and the principal antioxidant that mitigates these ROS remain unknown. Peroxiredoxin III (PrxIII) is the most abundant and potent H2O2-eliminating enzyme in the mitochondria of mammalian cells. Here, we investigated the role of mitochondrial H2O2 and the protective function of PrxIII in diclofenac-induced mitochondrial dysfunction and apoptosis in hepatocytes. Mitochondrial H2O2 levels were differentiated from other types of ROS using a fluorescent H2O2 indicator. Upon diclofenac treatment, PrxIII-knockdown HepG2 human hepatoma cells showed higher levels of mitochondrial H2O2 than PrxIII-expressing controls. PrxIII-depleted cells exhibited higher mitochondrial dysfunction as measured by a lower oxygen consumption rate, loss of mitochondrial membrane potential, cardiolipin oxidation, and caspase activation, and were more sensitive to apoptosis. Ectopic expression of mitochondrially targeted catalase in PrxIII-knockdown HepG2 cells or in primary hepatocytes derived from PrxIII-knockout mice suppressed the diclofenac-induced accumulation of mitochondrial H2O2 and decreased apoptosis. Thus, we demonstrated that mitochondrial H2O2 is a key mediator of diclofenac-induced hepatocellular damage driven by mitochondrial dysfunction and apoptosis. We showed that PrxIII loss results in the critical accumulation of mitochondrial H2O2 and increases the harmful effects of diclofenac. PrxIII or other antioxidants targeting mitochondrial H2O2 could be explored as potential therapeutic agents to protect against the hepatotoxicity associated with NSAID use.
8

Heikaus, Sebastian, Linda van den Berg, Tobias Kempf, Csaba Mahotka, Helmut Erich Gabbert, and Uwe Ramp. "HA14-1 is Able to Reconstitute the Impaired Mitochondrial Pathway of Apoptosis in Renal Cell Carcinoma Cell Lines." Analytical Cellular Pathology 30, no. 5 (January 1, 2008): 419–33. http://dx.doi.org/10.1155/2008/693095.

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Renal cell carcinomas (RCCs) exhibit a marked resistance towards apoptosis. Although most apoptotic stimuli converge at the level of the mitochondria, little is known about the mitochondrial apoptosis pathway in renal cell carcinomas. The aim of the present study, therefore, was to investigate the functionality of the mitochondrial apoptosis pathway in renal cell carcinoma cell lines by exposure to TRAIL, etoposide, HA14-1 and betulinic acid activating the mitochondria by different mechanisms. Sensitivity to TRAIL-induced apoptosis correlated with cleavage of the initiator caspase-8, but the mitochondrial apoptosis pathway was not induced. Similarly, etoposide and betulinic acid could not induce mitochondrial damage. In contrast, HA14-1 was able to activate mitochondrial apoptosis, thereby demonstrating functionally inducible signalling pathways downstream of the mitochondria. The intactness of the pathways upstream of the mitochondria was shown by pretreatment of TRAIL-sensitive cell lines with HA14-1, which could reconstitute TRAIL-induced mitochondrial damage and resulted in a synergistic apoptosis induction.Our results demonstrate that the apoptotic pathways upstream and downstream of the mitochondria are intact and inducible in renal cell carcinoma cell lines. However, resistance towards mitochondrial apoptosis is located on the level of the mitochondria themselves.
9

Peterson, Courtney M., Darcy L. Johannsen, and Eric Ravussin. "Skeletal Muscle Mitochondria and Aging: A Review." Journal of Aging Research 2012 (2012): 1–20. http://dx.doi.org/10.1155/2012/194821.

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Aging is characterized by a progressive loss of muscle mass and muscle strength. Declines in skeletal muscle mitochondria are thought to play a primary role in this process. Mitochondria are the major producers of reactive oxygen species, which damage DNA, proteins, and lipids if not rapidly quenched. Animal and human studies typically show that skeletal muscle mitochondria are altered with aging, including increased mutations in mitochondrial DNA, decreased activity of some mitochondrial enzymes, altered respiration with reduced maximal capacity at least in sedentary individuals, and reduced total mitochondrial content with increased morphological changes. However, there has been much controversy over measurements of mitochondrial energy production, which may largely be explained by differences in approach and by whether physical activity is controlled for. These changes may in turn alter mitochondrial dynamics, such as fusion and fission rates, and mitochondrially induced apoptosis, which may also lead to net muscle fiber loss and age-related sarcopenia. Fortunately, strategies such as exercise and caloric restriction that reduce oxidative damage also improve mitochondrial function. While these strategies may not completely prevent the primary effects of aging, they may help to attenuate the rate of decline.
10

Kroemer, Guido. "Heat Shock Protein 70 Neutralizes Apoptosis-Inducing Factor." Scientific World JOURNAL 1 (2001): 590–92. http://dx.doi.org/10.1100/tsw.2001.322.

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Programmed cell death (apoptosis) is the physiological process responsible for the demise of superfluous, aged, damaged, mutated, and ectopic cells. Its normal function is essential both for embryonic development and for maintenance of adult tissue homeostasis. Deficient apoptosis participates in cancerogenesis, whereas excessive apoptosis leads to unwarranted cell loss accounting for disparate diseases including neurodegeneration and AIDS. One critical step in the process of apoptosis consists in the permeabilization of mitochondrial membranes, leading to the release of proteins which normally are secluded behind the outer mitochondrial membrane[1]. For example, cytochrome c, which is normally confined to the mitochondrial intermembrane space, is liberated from mitochondria and interacts with a cytosolic protein, Apaf-1, causing its oligomerization and constitution of the so-called apoptosome, a protein complex which activates a specific class of cysteine proteases, the caspases[2]. Another example concerns the so-called apoptosis-inducing factor (AIF), another mitochondrial intermembrane protein which can translocate to the nucleus where it induces chromatin condensation and DNA fragmentation[3].
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Статті в журналах Дисертації Книги

Дисертації з теми "Apoptose mitochondriale":

1

Aure, Karine. "Physiopathologie moléculaire et cellulaire des maladies mitochondriales à présentation neurologique." Paris 6, 2007. http://www.theses.fr/2007PA066281.

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Les maladies mitochondriales sont liées à un déficit de la chaîne respiratoire mitochondriale. Ces maladies posent des problèmes de diagnostic, dans leurs relations phénotype/génotype et dans leurs mécanismes physiopathologiques. L'étude longitudinale d'un cas de déficit en ubiquinone a démontré les limites de la supplémentation thérapeutique. L'analyse de l’histoire naturelle et des caractéristiques moléculaires de 69 patients porteurs de délétion de l’ADN mitochondrial a permis d'établir une nouvelle classification clinique et des facteurs pronostiques. L’efficacité de l’immortalisation par le gène de la télomérase a été démontrée dans les fibroblastes déficitaires. Nous avons montré la présence d’apoptose dans le muscle de patients avec mutations de l'ADN mitochondrial. Les difficultés de la démonstration du pouvoir délétère des mutations homoplasmiques de l’ADN mitochondrial ont été abordées à travers l'étude de familles portant la même mutation de l'ARN de transfert de la proline.
2

Landes, Thomas. "Dynamique mitochondriale et apoptose : rôle de l'interaction entre Opa1 et Bnip3." Toulouse 3, 2009. http://thesesups.ups-tlse.fr/671/.

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La morphologie mitochondriale résulte d'un équilibre dynamique entre des évènements de fission et de fusion des membranes mitochondriales. Des données dans la littérature indiquent une relation étroite entre la dynamique mitochondriale et l'activation de la voie mitochondriale de l'apoptose qui consiste, via l'action des protéines de la famille de Bcl-2, en la perméabilisation de la membrane externe mitochondriale et au relargage de molécules apoptogènes, dont le cytochrome c, de l'espace inter-membranaire vers le cytoplasme. Ces dernières années, nos travaux nous ont conduit à isoler Opa1, une protéine indispensable à la fusion de la membrane interne mitochondriale. L'oligomérisation de cette dynamine a plus récemment été impliquée dans le contrôle de la conformation des crêtes mitochondriales, structures renfermant la majeure partie du cytochrome c. Afin de mieux appréhender ces deux fonctions de la protéine, une recherche de partenaires a été réalisée, au laboratoire, par une approche de double hybride chez la levure. Mon travail de thèse s'est focalisé sur la caractérisation physique et fonctionnelle de l'interaction entre Opa1 et l'un de ses partenaires, Bnip3, un membre pro-apoptotique de la famille de Bcl-2. Cette étude apporte des éléments déterminants pour la compréhension de la relation entre dynamique mitochondriale et apoptose et pourrait à terme être capital dans l'élucidation des mécanismes physiopathologiques de l'atrophie optique dominante de type 1, causée par des mutations du gène codant pour Opa1
Mitochondria are highly dynamic organelles that continually fuse and divide. Several studies suggest a link between mitochondrial dynamics and the intrinsic pathway of apoptosis, mediated by members of the Bcl-2 family, leading to the release of apoptogenic proteins, including cytochrome c, from the mitochondrial intermembrane space into the cytosol. We have previously identified Opa1 a dynamin of the inner membrane that regulates mitochondrial fusion. More recently, Opa1 has also been proposed to control, during apoptosis, cytochrome c redistribution through its capacity to locally form oligomers at mitochondrial cristae junctions. In this study, we identified Bnip3, a mitochondrial pro-apoptotic BH3-only protein of the Bcl-2 family, as a physical and functional partner of Opa1. Overall, our results give some insight into the relationship between mitochondrial dynamics and apoptosis and, in the future, may help to understand the aetiology of autosomal dominant optic atrophy, caused by Opa1 mutations
3

Desbourdes, Céline. "Nucléoside diphosphate kinase D : une protéine mitochondriale bifonctionnelle." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV004/document.

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Les nucléosides diphosphate kinases (NDPK) sont essentielles pour la génération des nucléosides triphosphates (NTPs) en utilisant l’ATP et des NDPs. L’isoforme mitochondriale de NDPK (NDPK-D), située dans l’espace intermembranaire des mitochondries, possède deux modes de fonctionnement. Dans le premier mode (« phosphotransfert »), la protéine a une activité de kinase comme les autres enzymes NDPK. Dans ce mode de fonctionnement, NDPK-D produit du GTP pour la protéine optique atrophy 1 (OPA1), une GTPase impliquée dans la fusion des mitochondries, et de l’ADP pour le translocateur à adénine (ANT) et l’ATPase mitochondriale pour la régénération d’ATP. Le second mode de fonctionnement est appelé « transfert de lipide » et est lié à la capacité de la protéine à se lier aux phospholipides anioniques, particulièrement la cardiolipine (CL). Dans ce mode NDPK-D peut réticuler les deux membranes mitochondriales et transférer CL de la membrane interne vers la membrane externe des mitochondries, pouvant servir de signal pour la mitophagie et l’apoptose. Ce travail a pour objectif d’étudier plus en détails ces différentes fonctions de NDPK-D. En utilisant des cellules HeLa exprimant de façon stable la protéine sauvage, kinase inactive (mutation H151N) ou incapable de se lier aux lipides (mutation R90D) et des cellules épithéliales de poumons de souris, nous montrons (i) une grande proximité entre NDPK-D et OPA1 qui conduit au channeling de GTP par NDPK-D pour OPA1, (ii) le rôle essentiel de NDPK-D pour l’externalisation de CL vers la surface des mitochondries pendant la mitophagie, servant de signal de reconnaissance pour le complexe LC3-II-autophagosomes afin d’éliminer les mitochondries endommagées, (iii) la possible inhibition de l’externalisation de CL par la présence de complexes NDPK-D/OPA1, et (iv) un phénotype pro-métastatique des cellules HeLa exprimant la NDPK-D mutée (H151N ou R90D), caractérisé par un fort potentiel invasif et migratoire, un profil protéique altéré, et des modifications au niveau structural et fonctionnel du réseau mitochondrial. Finalement, une première stratégie d’expression et de purification de la protéine OPA1 entière a été établie pour de futures études in vitro des complexes NDPK-D/OPA1
The nucleoside diphosphate kinases (NDPK) are essential for generation of nucleoside triphosphates (NTPs) using ATP and NDPs. The mitochondrial NDPK isoform (NDPK-D) located in the mitochondrial intermembrane space is found to have two modes of function. First, the phosphotransfer mode in which the protein has a kinase activity like other NDPK enzymes. In this mode, NDPK-D produces GTP for the optic atrophy 1 protein (OPA1), a GTPase involved in mitochondrial fusion, and ADP for the adenylate translocator (ANT) and the mitochondrial ATPase for ATP regeneration. The second mode of function is called lipid transfer and is related to the capacity of NDPK-D to bind anionic phospholipids, especially cardiolipin (CL). In this mode, the protein can cross-link the two mitochondrial membranes and transfer CL from the inner to the outer mitochondrial membrane, which can serve as a signal for mitophagy and apoptosis. This work aims to study these NDPK-D functions in more detail. With the use of HeLa cells stably expressing the wild-type, kinase inactive (H151N mutation) or lipid binding deficient (R90D mutation) NDPK-D and mouse lung epithelial cells, we show (i) the close proximity between NDPK-D and OPA1 that leads to GTP channeling from NDPK-D to OPA1, (ii) the essential role of NDPK-D for CL externalization to the mitochondrial surface during mitophagy, serving as a recognition signal for LC3-II-autophagosomes to eliminate damaged mitochondria, (iii) the possible inhibition of CL externalization due to the presence of NDPK-D/OPA1 complexes, and (iv) a pro-metastatic phenotype of HeLa cells expressing either of the NDPK-D mutants (H151N or R90D), characterized by high invasive and migratory potential, altered proteomic profile and changed mitochondrial network structure and function. Finally, a first bacterial expression and purification strategy for full-length OPA1 has been established for future in vitro studies of NDPK-D/OPA1 complexes
4

Olichon, Aurélien. "Morphologie mitochondriale : fonctions et dysfonctions de la dynamine humaine OPA1." Toulouse 3, 2004. http://www.theses.fr/2004TOU30295.

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Les mitochondries sont des organelles impliqués dans la production d'énergie et participent au à la mort cellulaire programmée ou apoptose. La structure et la dynamique de ces organelles à double membrane sont régulées par fusion ou fission membranaire. La fusion et la fission de la membrane externe sont respectivement assurées par la GTPase Fzo1/Mfn1-2 et la dynamine Dnm1/DRP. La dynamique de la membrane interne mitochondriale n'est pas encore connue. Toutefois, chez S. Cerevisiae, Mgm1p, et chez S. Pombe, Msp1 sont impliquées dans la dynamique du réseau mitochondrial. Leur localisation intra-mitochondriale suggère un rôle dans la dynamique de la membrane interne. OPA1, homologue humain de Msp1/Mgm1p, complémente la délétion du gène msp1 chez S. Pombe. Par une combinaison d'approches cytologiques et biochimiques nous avons montré en outre qu'OPA1 est une protéine fortement associée à la membrane interne mitochondriale, faisant face à l'espace inter-membranaire. J'ai analysé l'effet de l'inhibition de l'expression de OPA1 par interférence ARN. L'invalidation d'OPA1 provoque une fragmentation du réseau mitochondrial, une dissipation du potentiel de membrane DYm et est suivie de la mort des cellules par apoptose par relargage du cytochrome c. Par des approches de surexpression ou d'interférence ARN sélective des variant d'épissage d'OPA1, j'ai pu montrer que l'épissage alternatif permet de dissocier les fonctions d'OPA1 impliquées dans la morphologie du réseau mitochondrial de celles responsables de la mort cellulaire. Des mutations du gène codant pour OPA1 sont responsables de l'atrophie optique dominante de type 1 (ADOA, MIM 165500) conduisant à une neuro-dégénérescence des cellules ganglionnaires de la rétine (RGC) suivie d'une atrophie du nerf optique aboutissant à la cécité. J'ai caractérisé deux mutants pathogènes d'OPA1, et montré que la pathogénicité associée aux mutations d'OPA1 pourrait résulter aussi bien d'effets dominants négatifs que d'haplo-insuffisance
Mitochondria are essential organelles that provide energy to the cell and act as reservoirs of apoptogenic molecules. Mitochondrial morphology and dynamics are crucial for their function and their transmission, and drastically change during apoptosis. To explain the dynamic of the mitochondrial network morphology, a model conserved from yeast to human proposes that two antagonistic forces, fission versus fusion, are monitored by proteins localized on the mitochondrial outer membrane, such as Dnm1/DRP-1 or Fzo1/Mfn1-2. Conversely, dynamic of the inner membrane is largely unknown. Data on the large GTPase Msp1 in S. Pombe, OPA1 in human, and Mgm1 in S. Cerevisiae suggest that this dynamin related protein is involved in the inner-membrane structure and dynamic. We have isolated the OPA1 gene sequence encoding a human dynamin. Moreover, we have shown that OPA1 gene is mutated in patients suffering from an hereditary optic neuropathy leading to blindness (ADOA: Autosomal Dominant Optic Atrophy, OMIM 165500) My thesis project was to characterize OPA1 function in order to understand its dysfunction, impact on mitochondrial dynamics and function, and especially answer some questions about the pathological process of the ADOA. Orthology between OPA1 and Msp1 was confirmed by showing that OPA1 complements the lethal msp1 gene deletion in fission yeast. Using both biochemical and cytological approaches we have precisely localized OPA1 strongly associated with the inner membrane of the mitochondria, facing the innermembrane space. To investigate OPA1 dynamin function, we used total or selective downregulation or over-expression of wild type OPA1 variants or mutant, and showed that OPA1 could function in the inner-membrane dynamics and could have a role in structuring the cristae membrane. This later structural role suggests that OPA1 could be a key regulator of the mobilization of cytochrome c by remodeling the cristae membrane
5

Singh, François. "Skeletal muscle toxicity and statins : role of mitochondrial adaptations." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ050/document.

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Bien que les statines forment la classe d'hypolipidémiants la plus utilisée, une toxicité musculaire a été reportée, pouvant ainsi provoquer l’apparition d’une myopathie. Dans la première partie, nous avons montré chez l’Homme et l’animal que les statines inhibent directement la chaine respiratoire mitochondriale, et induisent la production de radicaux libres dérivés de l’oxygène (RLO), qui active les voies apoptotiques dans les muscles glycolytiques, alors que les muscles oxydatifs ne sont pas atteints. Nous avons ensuite montré in vitro que le stress réducteur peut engendrer une oxydation mitochondriale, pouvant conduire à une activation de la voie de biogenèse mitochondriale. De plus l’augmentation du contenu mitochondrial induite a permis de protéger les cellules contre l’apoptose induite par les statines. Enfin, nous avons montré in vivo que l’induction des voies de biogenèse mitochondriale est nécessaire à la tolérance des statines dans les muscles oxydatifs. En conclusion, le phénotype mitochondrial, tant au niveau quantitatif que qualitatif, semble être un facteur clé dans l’apparition de la myopathie aux statines
Although statins are the most prescribed class of lipid-lowering agents, adverse muscular toxicity has been reported, which can lead to the appearance of a myopathy. In the first part, we showed in Humans and animals that statins inhibit directly the mitochondrial respiratory chain, and induce the production of reactive oxygen species (ROS), that trigger apoptotic pathways in glycolytic skeletal muscles, whereas oxidative muscles are not impaired. We then showed in vitro that reductive stress can provoke mitochondrial oxidation, that could lead to an activation of mitochondrial biogenesis pathways. Moreover, the consequent increase in mitochondrial content enabled to protect cells against statin-induced apoptosis. Finally, we showed in vivo that the induction of mitochondrial biogenesis is necessary for statin tolerance in oxidative skeletal muscles. In conclusion, mitochondrial phenotype, both quantitatively and qualitatively, seems to be a key factor in the appearance of statin myopathy
6

Ferré, Cécile. "Mécanismes moléculaires et cellulaires à la base du pouvoir neuroprotecteur de la protéine "mitochondriale" X du bornavirus." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30049/document.

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Les maladies neurodégénératives constituent un enjeu humain, sociétal et économique majeur, dont l'importance croît avec le vieillissement des populations. Cette dénomination regroupe un grand nombre de maladies neurologiques, comme les maladies d'Alzheimer, de Parkinson ou la sclérose latérale amyotrophique (SLA). L'étiologie de ces maladies est complexe et reste encore mal comprise. Néanmoins, elles résultent vraisemblablement d'une combinaison de facteurs génétiques et environnementaux et se caractérisent toutes par la dégénérescence d'une population neuronale spécifique. Les mitochondries jouent un rôle primordial dans l'apport énergétique, la régulation calcique ou la gestion du stress cellulaire et sont directement impliquées dans le déclenchement de la mort cellulaire programmée (ou apoptose). L'implication centrale de cet organite dans les pathologies neurodégénératives a logiquement suscité un ciblage croissant des fonctions mitochondriales dans les nouvelles approches thérapeutiques envisagées ces dernières années. Des curcuminoïdes ont par exemple été testés pour contrer les effets dus au stress oxydatif, mais les résultats restent encore à être améliorés. L'utilisation de facteurs anti-apoptotiques dérivés de virus représente une piste très prometteuse. En effet, l'apoptose des cellules infectées représente la "première ligne" de défense de l'hôte contre une invasion virale. En réponse à ce mécanisme de défense, de nombreux virus expriment divers facteurs (protéines, ARN ...) dont la fonction est de bloquer le processus apoptotique, en particulier en ciblant la mitochondrie, favorisant ainsi la réplication virale au sein de la cellule. Dans ce contexte, notre équipe a établi que la protéine X du Bornavirus possède de remarquables propriétés neuroprotectrices. Si le potentiel thérapeutique de cette protéine virale est maintenant démontré, les mécanismes moléculaires à l'origine de cet effet neuroprotecteur étaient à ce jour inconnus. Au cours de ma thèse, nous avons contribué à une meilleure compréhension de la biologie de cette protéine au sein de la cellule et en particulier dans les mitochondries. Nous avons déterminé ses séquences d'adressages intracellulaires ainsi que son impact sur la dynamique mitochondriale et sur certains paramètres de la bioénergétique mitochondriale tels que le potentiel de membrane mitochondrial, la respiration cellulaire et la production d'ATP (énergie de nos cellules). L'ensemble de ces connaissances devrait nous permettre d'améliorer sa capacité neuroprotectrice
Bornavirus, a non-cytolytic RNA virus establishes a long-lasting persistence in the central nervous system of infected animals. Viral persistence is facilitated by the expression of the non-structural X protein, which is addressed both to nucleus and mitochondria, where it interferes both with cellular antiviral responses and the initiation of apoptosis. Our team recently reported that the singled-out expression of the X protein could protect neurons against toxins of the mitochondrial respiratory chain, both in vitro and in a mouse model of Parkinson's disease (PD). During my Ph.D., we further demonstrated that the X protein triggered enhanced filamentation of the mitochondrial network, in physiological as well as in oxidative stress conditions. This effect is particularly interesting when considering the importance of mitochondrial dynamics in the pathophysiology of neurodegenerative diseases. Even if the therapeutic potential of this viral protein is now well established, the underlying molecular and cellular mechanisms are far from being elucidated. It is however clear that neuroprotection conferred by the X protein is strictly dependent on its mitochondrial localization. In this context, the goal of my Ph.D. project was to clarify the molecular mechanisms whereby the X protein is targeted to mitochondria and/or to the nucleus, in link with its protective capabilities. We focused on the amino terminal residues of X, by performing fusion proteins of various forms of these residues with GFP and by analyzing their cellular localization. We demonstrated that this region contains overlapping and interdependent signals for nuclear localization, nuclear export and mitochondrial targeting of the X protein. We also identified a point mutation or deletion leading to an almost exclusively mitochondrial localization of the X protein. As a consequence, these X mutants exhibited a better neuroprotective function. In order to get further insight into X-mediated neuroprotection, we also searched for the cellular partners of X in mitochondria. We revealed a direct and specific interaction of the X protein with the chaperone Hspa9, a protein that was recently shown to be involved in neurodegenerative diseases, notably in PD's patients. We observed that the down-regulation of Hspa9 triggered by mitochondrial toxins was attenuated by the coexpression of X, suggesting a functional link between these two proteins. We also demonstrated that Hspa9 overexpression could protect neurons from mitochondrial dysfunctions, similarly to the X protein. Altogether, these results have contributed to a better understanding of the mechanisms underlying the neuroprotective potential of the X protein, which may favor the development of novel therapeutic strategies
7

Carré, Manon. "Agents anti-tubuline et apoptose : du cytosquelette microtubulaire à la tubuline mitochondriale." Aix-Marseille 2, 2004. http://www.theses.fr/2004AIX22955.

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8

Martel, Cécile. "Rôle de la perméabilité membranaire mitochondriale, de la phosphorylation de VDAC et de la signalisation de l’apoptose dans la pathogenèse de la stéatose hépatique." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T075.

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La stéatose hépatique non-alcoolique consiste en une accumulation de lipides dans le cytoplasme des hépatocytes. Longtemps considérée comme une pathologie bénigne, elle peut être à l’origine du développement d’un stade plus sévère : la stéatohépatite non alcoolique (NASH). La NASH s’accompagne de lésions sévères du foie liées à la genèse d’un stress oxydant, d’une inflammation et de la mort cellulaire. Le rôle de la mitochondrie est au centre de cette maladie, bien que les connaissances sur la dysfonction mitochondriale et ses conséquences sur l’apoptose soient encore insuffisantes. En effet, la mitochondrie est responsable de la dégradation des lipides par -oxydation et elle agit comme un centre intégrateur des signaux apoptotiques en déclenchant une perméabilisation des membranes mitochondriales (PMM) aboutissant à la libération de facteurs apoptogènes. Ce processus est considéré comme le point de non-retour de la voie mitochondriale de l’apoptose. Nos travaux ont porté sur la compréhension des mécanismes moléculaires liant l’apoptose hépatocytaire mitochondriale et la stéatose. La combinaison de quatre modèles expérimentaux de stéatose (biopsies de patients, mitochondries isolées de souris obèses ob/ob ou recevant un régime hypercalorique, et lignées cellulaires) a permis de montrer, dans le foie stéatosique, une sensibilité accrue à l’induction de la PMM et une augmentation de la perméabilité de VDAC (voltage-dependent anion channel), protéine formant un canal dans la membrane externe mitochondriale. Ces observations sont associées à une diminution de la phosphorylation de VDAC sur un résidu thréonine et sa perte d’interaction avec la protéine anti-apoptotique Bcl-XL et la kinase GSK3, révélant ainsi une nouvelle voie de signalisation par les lipides. Cette découverte s’est notamment appuyée sur l’utilisation de tests fonctionnels en mitochondries isolées que nous avions développés et validés dans plusieurs études aux stratégies expérimentales variées. En conclusion, notre étude permet de mieux comprendre la fragilité mitochondriale lipo-induite, stade précédant l’apoptose hépatocytaire, et ouvre des perspectives à visée biomédicale
Non-alcoholic steatosis is a liver disease characterized by lipid accumulation in the cytoplasm of hepatocytes. For a long time, it has been considered as a benign condition. Now it is known that it can precede the development of a severe stage, non-alcoholic steatohepatitis (NASH). NASH is accompanied by severe dammages of the liver linked to the genesis of oxidative stress, inflammation and cell death. Mitochondrion is a central player of this disease; however, the knowledge of mitochondrial dysfunction and its consequences on apoptosis is still insufficient. Indeed, mitochondria are responsible for lipid degradation by -oxidation. Mitochondria act as a central integrator of apoptotic signals by triggering the mitochondrial membrane permeabilization (MMP) leading to the release of apoptogenic factors. This process is considered as the point of no return of the mitochondrial pathway of apoptosis. We aimed to better understand the molecular mechanisms linking mitochondrial liver apoptosis and steatosis. Combination of four experimental models of steatosis (human biopsies, isolated mitochondria from ob/ob obese mice, high fat diet-fed mice or hepatic cell lines) displayed, in steatotic livers, increased sensitivity to MMP induction and permeability of VDAC (Voltage dependent anion channel), a protein which forms a channel in the outer mitochondrial membrane. These findings are associated with the hypo-phosphorylation of VDAC on a threonine residue and the loss of its interaction with the anti-apoptotic Bcl-XL and GSK3 kinase, thus revealing a new lipid-induced signaling pathway. Our work is based on the use of functional assays on isolated mitochondria that we have developed and validated in several studies involving various strategies. To conclude, our study increases the knowledge on the lipid-induced mitochondrial weakness preceding hepatic apoptosis and opens perspectives in biomedical applications
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Jelinek, Antje. "In-vitro-Toxizität grenzflächenaktiver Substanzen Wirkung auf Zellmembran, mitochondriale Funktion und Apoptose /." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963587676.

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10

Lefevre, Sophie. "Modèle levure de l'ataxie de Friedreich : stress oxydant, apoptose et dynamique mitochondriale." Paris 6, 2010. http://www.theses.fr/2010PA066204.

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Книги з теми "Apoptose mitochondriale":

1

Joza, Nicholas. Differential requirement for the mitochondrial apoptosis-inducing factor in apoptotic pathways. Ottawa: National Library of Canada, 2001.

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2

Wadia, Jehangir S. R(-)-deprenyl treatment blocks apoptosis in PC12 cells by affecting mitochondrial membrane potential, mitochondrial calcium and superoxide radical generation. Ottawa: National Library of Canada, 1996.

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3

Saavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Hauppauge, N.Y: Nova Science Publishers, 2010.

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4

Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer, 2011.

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Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer, 2011.

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Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer London, Limited, 2012.

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7

Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Edited by Patrick Lestienne. SPRINGER-VERLAG, 1999.

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Wadia, J. S. Changes in mitochondrial protein import during apoptosis. 2002.

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9

(Editor), Guy C. Brown, David G. Nicholls (Editor), and Chris E. Cooper (Editor), eds. Mitochondria and Cell Death. Princeton University Press, 1999.

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10

Lee, Hong Kyu, Salvatore DiMauro, Masashi Tanaka, and Yau-Huei Wei. Mitochondrial Pathogenesis: From Genes and Apoptosis to Aging and Disease. Springer London, Limited, 2014.

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Частини книг з теми "Apoptose mitochondriale":

1

Mignotte, B., and G. Kroemer. "Roles of Mitochondria in Apoptosis." In Mitochondrial Diseases, 239–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_18.

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Peluso, G., O. Petillo, S. Margarucci, A. Calarco, and M. Calvani. "Deregulation of Mitochondrial Apoptosis in Cancer." In Mitochondrial Disorders, 71–87. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0929-8_7.

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3

Lee, Myung-Shik, Ja-Young Kim, and Sun Young Park. "Resistance of ρ0 Cells against Apoptosis." In Mitochondrial Pathogenesis, 146–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2_15.

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Servidei, S., S. Di Giovanni, A. Broccolini, A. D’amico, M. Mirabella, and G. Silvestri. "Apoptosis and Oxidative Stress in Mitochondrial Disorders." In Mitochondrial Disorders, 37–45. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0929-8_4.

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5

Antonsson, Bruno. "The Mitochondrial Apoptosis Pathway." In Essentials of Apoptosis, 85–99. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-361-3_6.

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6

Cleland, Megan M., and Richard J. Youle. "Mitochondrial Dynamics and Apoptosis." In Mitochondrial Dynamics and Neurodegeneration, 109–38. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1291-1_4.

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7

Fernández-Checa, Jose C., and Carmen Garcia-Ruiz. "Apoptosis and Mitochondria." In Signaling Pathways in Liver Diseases, 439–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_29.

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Petit, Patrice Xavier, Naoufal Zamzami, Jean-Luc Vayssière, Bernard Mignotte, Guido Kroemer, and Maria Castedo. "Implication of mitochondria in apoptosis." In Detection of Mitochondrial Diseases, 185–88. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8_28.

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9

Petit, Patrice X., and Guido Kroemer. "Mitochondrial Regulation of Apoptosis." In Mitochondrial DNA Mutations in Aging, Disease and Cancer, 147–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-12509-0_8.

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El-Osta, Hazem, and Magdalena L. Circu. "Mitochondrial ROS and Apoptosis." In Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease, 1–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42139-1_1.

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Тези доповідей конференцій з теми "Apoptose mitochondriale":

1

Kichkina, D. O., S. S. Patrushev, A. D. Moralev, E. E. Shults, M. A. Zenkova, and A. V. Markov. "NEW SEMISYNTHETIC SESQUITERPENE LACTONES AS INDUCERS OF OXIDATIVE STRESS IN TUMOR CELLS AND BLOCKERS OF THE AGGRESSIVE PHENOTYPE OF GLIOBLASTOMA MULTIFORME CELLS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-331.

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Screening for the antitumor potency of novel derivatives of isoalanotlactone revealed: (1) compound pat_651p, demonstrating high selectivity of action in respect to tumor cells and triggering oxidative stress and mitochondrial-dependent apoptosis in them; (2) compound pat_651_6p capable of passing through the blood-brain barrier and effectively inhibiting the motility, invasion, and adhesive traits of glioblastoma multiforme cells.
2

Liu, G., S. Soberanes, N. Bruce, SA Weitzman, GR Budinger, PT Schumacker, and DW Kamp. "A Mitochondria-Targeted DNA Repair Enzyme, hOgg1, Prevents Oxidant-Induced Alveolar Epithelial Cell Apoptosis by Chaperoning and Preserving Mitochondrial Aconitase." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4178.

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3

Luo, Yu, Zhuoyan Zhang, and David Kessel. "Role of mitochondrial photodamage in PDT-induced apoptosis." In BiOS '98 International Biomedical Optics Symposium, edited by Thomas J. Dougherty. SPIE, 1998. http://dx.doi.org/10.1117/12.308138.

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Pourzia, Alexandra, Michael Olson, Stefanie Bailey, Aditi Aryal, Jeremy Ryan, Marcela Maus, and Anthony Letai MD. "269 Mitochondrial apoptosis mediates CAR T cell cytotoxicity." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0269.

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5

Hamacher-Brady, Anne, Verena Lang, and Nathan R. Brady. "Abstract 3324: FATE1 promotes mitochondrial hyperfusion and supports maintenance of mitochondrial networks following apoptosis stimulation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3324.

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6

Zebo, Tang, Liu Yanbo, Li Chun, Wen Na, and Gai Xiaodong. "pLXSN-Tum-5 inducing HUVEC apoptosis through mitochondrial pathway." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027904.

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7

Lee, Yuan-Hao, Exing Wang, Neeru Kumar, and Randolph D. Glickman. "Ursolic acid mediates photosensitization by initiating mitochondrial-dependent apoptosis." In SPIE BiOS, edited by E. Duco Jansen and Robert J. Thomas. SPIE, 2013. http://dx.doi.org/10.1117/12.2000225.

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8

Zhuang, Cai-ping, Qian Liang, Xiao-ping Wang, and Tong-sheng Chen. "Hydrogen peroxide induces apoptosis via a mitochondrial pathway in chondrocytes." In SPIE BiOS, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2012. http://dx.doi.org/10.1117/12.905786.

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9

Sui, Cliff, and Nada Boustany. "Potential application of the FDTD technique to study mitochondrial apoptosis." In Biomedical Optics (BiOS) 2007, edited by Adam Wax and Vadim Backman. SPIE, 2007. http://dx.doi.org/10.1117/12.702151.

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10

Kamp, David, Paul Cheresh, Humberto Trejo, Katie Knister, Jing Liu, and Anna Lam. "Asbestos-Induced Alveolar Epithelial Cell Apoptosis: Mitochondria-ER Crosstalk." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4277.

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Звіти організацій з теми "Apoptose mitochondriale":

1

Myers, Charles. Mitochondrial Apoptosis: A New Foundation for Combining Agents in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada402436.

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2

Tweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality,Apoptosis, Inflammation and Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada612817.

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3

Tweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality, Apoptosis, Inflammation and Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, December 2012. http://dx.doi.org/10.21236/ada612818.

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4

Myers, Charles E. Mitochondrial Apoptosis: A New Foundation for Combing Agents in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, March 2000. http://dx.doi.org/10.21236/ada392324.

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5

Tweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality, Apoptosis, Inflammation and Mitochondrial Dysfunction Using IL-6 as a Resuscitation Adjuvant. Fort Belvoir, VA: Defense Technical Information Center, December 2011. http://dx.doi.org/10.21236/ada612819.

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