The role of mitochondria in apoptosis.

By Seon-Yong Jeong, D. Seol. BMB Reports, 2008

1,415 citations recorded by the source corpus.

Apoptosis (programmed cell death) is a cellular self-destruction mechanism that is essential for a variety of biological events, such as developmental sculpturing, tissue homeostasis, and the removal of unwanted cells. Mitochondria play a crucial role in regulating cell death. Ca2+ has long been recognized as a participant in apoptotic pathways. Mitochondria are known to modulate and synchronize Ca2+ signaling. Massive accumulation of Ca2+ in the mitochondria leads to apoptosis. The Ca2+ dynamics of ER and mitochondria appear to be modulated by the Bcl-2 family proteins, key factors involved in apoptosis. The number and morphology of mitochondria are precisely controlled through mitochondrial fusion and fission process by numerous mitochondria-shaping proteins. Mitochondrial fission accompanies apoptotic cell death and appears to be important for progression of the apoptotic pathway. Here, we highlight and discuss the role of mitochondrial calcium handling and mitochondrial fusion and fission machinery in apoptosis.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/017c03f16552f415aed793416260b2a3c35cc5e7

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Citations in the corpus

• Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. (2012, neutral): “The mitochondrial pathway is triggered by the proapoptotic members of the Bcl-2 family of proteins that render the outer membrane of mitochondria permeable to factors normally located within the intermembrane space, in particular cytochrome c and Smac/ Diablo (Wang and Youle, 2009).”
• The Unfolded Protein Response and Cell Fate Control. (2017, positive): “…pathway, which is triggered when certain mitochondrial proteins, such as cytochrome c Molecular Cell 69, January 18, 2018 5 Review and Smac/Diablo, are forcibly released into the cytoplasmwhere they lead to activation of downstream effector caspases (e.g., caspase-3) (Wang and Youle, 2009).”
• The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways. (2012, neutral): “During apoptosis, cytochrome c, Smac/Diablo, Omi/HtrA2, EndoG, and AIF are released from the mitochondrial intermembrane space and elicit biochemical reactions leading to apoptosis (Wang and Youle, 2009).”
• Anti-apoptosis and cell survival: a review. (2011, background): “Mitochondrial derived activator of Caspase/Direct IAP-Binding protein with a LOw pI), the serine protease Omi/HtrA2, endonuclease G (EndoG) and apoptosis inducing factor (AIF) [12–14].”