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Review
. 2002 May;87(5):480-7.
doi: 10.1136/heart.87.5.480.

Apoptosis in the cardiovascular system

Martin R Bennett  1
Affiliations
Review

Apoptosis in the cardiovascular system

Martin R Bennett. Heart. 2002 May.
No abstract available

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Figures

Figure 1
Figure 1
Electron microscopic appearances of a human vascular smooth muscle cell (VSMC) undergoing apoptosis in culture. (A) Normal appearance of a human VSMC. VSMC also contains an apoptotic body (arrow). (B) Peripheral condensation of nuclear chromatin. (C) Intense membrane blebbing and vesicle formation in apoptosis, with condensation of the nuclear chromatin into clumps. (D) An apoptotic body, the end product of apoptosis.
Figure 2
Figure 2
Schematic of Fas death signalling pathways. Fas, the prototypic member of the tumour necrosis factor (TNF) death receptor family, binds to its cognate ligand. Recruitment of the adapter molecule FADD and pro-caspase 8 results in activation of the latter. Caspase 8 activation directly activates downstream caspases, (3, 6, and 7) which results in DNA fragmentation and cleavage of cellular proteins. This pathway is thought to occur in type I cells and does not involve mitochondrial pathways. Caspase 8 activation also results in cleavage of Bid, which translocates and interacts with other Bcl-2 family members (see fig 3).
Figure 3
Figure 3
Schematic of mitochondrial death signalling pathways. Anti-apoptotic members of the Bcl-2 family, such as Bcl-2 and Bcl-X, are located on the mitochondrial outer membrane. Here they act to prevent the release of apoptogenic factors from the inner mitochondrial space. Binding of the pro-apoptotic proteins Bid (after cleavage by caspase 8) or Bad (after dephosphorylation) to Bcl-2 mitigates the protective effect of Bcl-2 and triggers release of cytochrome c and Smac/DIABLO. Cytochrome c, in concert with the adapter protein apaf-1 and caspase 9, activates caspase 3 and the downstream caspase cascade. Smac/DIABLO inhibits IAPs (inhibitor of apoptosis proteins), which in turn inhibit caspase activities, thus propagating apoptosis. Stimuli such as growth factor withdrawal or activation of p53 and Fas activation in type II cells act through this mitochondrial pathway.
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References

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