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Fig. 9. Pathway of cardiac myocyte death by exposure to hypoxia–acidosis. Hypoxia mediates accumulation of hypoxia-inducible factor-1{alpha} (HIF-1{alpha}), and activated HIF-1 induces transcription of BNIP3. BNIP3 is loosely membrane bound at neutral pH but translocates into membranes, including mitochondria, when the pH decreases. Acidosis is caused by anaerobic metabolism. BNIP3 stimulates opening of the mitochondrial permeability transition pore (MPTP), releasing pro-apoptotic factors including apoptosis inducing factor (AIF), cytochrome c and calcium. Myocyte death, involving DNA fragmentation and nuclear condensation, requires MPTP opening but does not involve activation of caspases. The black box indicates that the proteases and DNases, presumed to be involved in cell death, are not yet identified. Broken lines indicate points where the death pathway can be blocked. Bongrekic acid (BA) and decylubiquinone (DUB) both inhibit MPTP opening and block myocyte death.





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