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FIGURE 3. Cytokine and oxidative stress (reactive oxygen species) in heart failure lead to caspase 3 activation by release of cytochrome c from mitochondria into cytoplasmic compartment. Activation of caspase 3 results in cytoplasmic proteolysis and DNA fragmentation and, hence, apoptosis. Endogenous upregulation of BCl2- and XIAP-like proteins and loss of DNA fragmentation factors prevent completion of apoptotic process (apoptosis interruptus). Amount of activated caspase 3 is determined by balance of antiapoptotic and proapoptotic factors. The fewer the endogenous antiapoptotic factors, the greater is the residual caspase, the PS externalization, the likelihood of an annexin-positive scan, and the necessity for apoptosis inhibition therapy and the poorer is the prognosis.
