Mitochondria in Apoptosis: Bcl-2 family Members and Mitochondrial Dynamics

By J. Martinou, R. Youle. Developmental Cell, 2011

1,375 citations recorded by the source corpus.

Mitochondria participate in apoptosis through a range of mechanisms that vary between vertebrates and invertebrates. In vertebrates, they release intermembrane space proteins, such as cytochrome c, to promote caspase activation in the cytosol. This process is the result of the loss of integrity of the outer mitochondrial membrane caused by proapoptotic members of the Bcl-2 family. This event is always accompanied by a fissioning of the organelle. Fission of mitochondria has also been reported to participate in apoptosis in Drosophila and Caenorhabditis elegans. However, in these organisms, mitochondrial membrane permeabilization does not occur and the mechanism by which mitochondrial dynamics participates in cell death remains elusive.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/83fcdbb81dfaea0c60c409304d3b8c9ea520c7ae

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Citations in the corpus

Programmed Cell Death in Animal Development and Disease (2011, neutral): “This facilitates MOMP and allows the release of cytochrome c (and other proteins from the intermembrane space) into the cytosol, resulting in the formation of the apoptosome (Martinou and Youle, 2011).”
The Role of the PERK/eIF2α/ATF4/CHOP Signaling Pathway in Tumor Progression During Endoplasmic Reticulum Stress (2016, background): “The proteins of the Bcl-2 family are well-characterized regulators of apoptotic cell death [85].”
Bax, Bak and beyond — mitochondrial performance in apoptosis (2018, background): “Mitochondrial composition, dynamics and interactions with other organelles have been shown to impact on the commitment to cell death, although the molecular mechanisms remain poorly defined [14-16].”
Mitochondria: In Sickness and in Health (2012, background): “Mitochondrial division and fusion also impinge on apoptosis by mechanisms that are not yet fully understood (Martinou and Youle, 2011).”
IRF4 Transcription Factor-Dependent CD11b+ Dendritic Cells in Human and Mouse Control Mucosal IL-17 Cytokine Responses (2013, methodology): “Because cells undergoing apoptosis show enhanced mitochondrial fission and fragmentation (Martinou and Youle, 2011), we performed a mitotracker assay that assessed mitochondrial network integrity in lung CD11b+ DCs lacking IRF4.”
Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “Apoptotic protease factor 1 (Apaf-1) was activated by this process, which is an essential step within the intrinsic pathway, resulting in the activation of procaspase-9.(114,115) The process of apoptosis leads to a dramatic reorganization of mitochondrial networks into punctate spheres rather than l”