Bid acts on the permeability transition pore complex to induce apoptosis

Zamzami, Naoufal; Hamel, Chahrazed El; Maisse, Carine; Brenner, Catherine; Muñoz-Pinedo, Cristina; Belzacq, Anne-Sophie; Costantini, Paola; Vieira, Helena L.A.; Loeffler, Markus; Molle, Gérard; Kroemer, Guido

doi:10.1038/sj.onc.1204030

Cited by 171 publications

(111 citation statements)

References 52 publications

(91 reference statements)

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“…18 Biochemical links between components traditionally viewed to form the PTP (e.g., VDAC or the ANT) and BCL-2 family members also strengthened the view that the role of the processes mediated by these two complexes of proteins were in some way coordinated, although many contradictory reports exist in the literature (e.g. [19][20][21][22][23] ). Later, it was reported that BCL-2 overexpression also inhibited the PTP-dependent release of apoptosis inducing factor from the intermembrane space.…”

Section: Bcl-2 and The Ptpmentioning

confidence: 99%

The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents?

Forte

Bernardi

2006

Cell Death Differ

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Section: Bcl-2 and The Ptpmentioning

confidence: 99%

The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents?

Forte

Bernardi

2006

Cell Death Differ

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“…Interestingly, cross-talk between the mPTP and Bcl-2 proteins has been described, with Bid and Bax promoting mPTP opening [41,42], while the antiapoptotic Bcl-2 and Bcl-X L possess an inhibitory effect [43]. …”

Section: Signaling Pathways Of Apoptotic Cell Deathmentioning

confidence: 99%

Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

Marzetti

Privitera

Simili

et al. 2010

The Scientific World JOURNAL

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Sarcopenia, the age-related decline in muscle mass and function, represents a significant health issue due to the high prevalence of frailty and disability associated with this condition. Nevertheless, the cellular mechanisms responsible for the loss of muscle mass in old age are still largely unknown. An altered regulation of myocyte apoptosis has recently emerged as a possible contributor to the pathogenesis of sarcopenia. Studies in animal models have shown that the severity of skeletal muscle apoptosis increases over the course of aging and correlates with the degree of muscle mass and strength decline. Several apoptotic pathways are operative in aged muscles, with the mitochondria- and TNF-α-mediated pathways likely being the most relevant to sarcopenia. However, despite the growing number of studies on the subject, a definite mechanistic link between myocyte apoptosis and age-related muscle atrophy has not yet been established. Furthermore, the evidence on the role played by apoptosis in human sarcopenia is still sparse. Clearly, further research is required to better define the involvement of myocyte apoptosis in the pathogenesis of muscle loss at advanced age. This knowledge will likely help in the design of more effective therapeutic strategies to preserve muscle mass into old age, thus fostering independence of the elderly population and reducing the socioeconomic burden associated with sarcopenia.

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“…Indeed, caspase-8 induces the proteolytic maturation of the BH3-only protein Bid, which, in its truncated form (tBid) translocates to mitochondria and favors MMP [21,26,27]. tBid acts at mitochondria through the cardiolipin-facilitated interaction with other pro-apoptotic members of the Bcl-2 family (e.g.…”

Section: Intrinsic and Extrinsic Apoptosis Pathwaysmentioning

confidence: 99%

Methods for the assessment of mitochondrial membrane permeabilization in apoptosis

et al. 2007

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Mitochondrial membrane permeabilization (MMP) is considered as the "point-of-no-return" in numerous models of programmed cell death. Indeed, mitochondria determine the intrinsic pathway of apoptosis, and play a major role in the extrinsic route as well. MMP affects the inner and outer mitochondrial membranes (IM and OM, respectively) to a variable degree. OM permeabilization culminates in the release of proteins that normally are confined in the mitochondrial intermembrane space (IMS), including caspase activators (e.g. cytochrome c) and caspase-independent death effectors (e.g. apoptosis-inducing factor). Partial IM permeabilization disrupts mitochondrial ion and volume homeostasis and dissipates the mitochondrial transmembrane potential ( m ). The assessment of early mitochondrial alterations allows for the identification of cells that are committed to die but have not displayed yet the apoptotic phenotype. Several

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Bid acts on the permeability transition pore complex to induce apoptosis

Cited by 171 publications

References 52 publications

The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents?

The permeability transition and BCL-2 family proteins in apoptosis: co-conspirators or independent agents?

Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging

Methods for the assessment of mitochondrial membrane permeabilization in apoptosis

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