FIGURE 2.

Overview of apoptosis and necrosis pathways following ICH. Oxidative stress, inflammatory cytokines (e.g., TNF), and Fas/Fas ligand after ICH may activate intrinsic caspase-dependent pathways to induce the emergence of mitochondrial membrane permeability (MMP). Cytochrome c is then released from mitochondria to activate caspases to initiate the process of cell death. Mechanical compression by the hematoma on adjacent tissue and activation of NMDAR by excessive glutamate after ICH can result in an influx of calcium, which causes mitochondrial dysfunction. Ultimately, cells go to die due to insufficient ATP produced by mitochondria. NMDAR, N-methyl-D-aspartate receptor; TNF, tumor necrosis factor; TNFR, TNF receptor; Bak, Bcl-2 homologous antagonist killer; Bax, Bcl-2 associated X protein; Ca²⁺, calcium ion; C, cytochrome c; Apaf-1, apoptotic protease-activating factor 1.