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. 2023 Feb 10;14:1138566. doi: 10.3389/fphar.2023.1138566

FIGURE 1.

FIGURE 1

The mechanism of mitochondrial dysfunction after CCH. CCH related excitotoxicity induced mPTP formation (A), which leads to calcium overload. Chronic hypoxia inhibits mitochondrial oxidative phosphorylation, resulting in excessive production of ROS, inhibition of ETC complex and antioxidant enzyme inactivation, eventually oxidative stress (B). Calcium overload and oxidative stress rupture mitochondrial outer membrane (C), trigger the release of pro-apoptotic factors (Cyt C and AIF) (D), which mediate Caspase cascade and DNA fragmentation, respectively, leading to apoptosis/cell death (E). Meanwhile, Bcl-2 family proteins play a key role in regulating the release of anti-apoptotic factors (D). Mitochondrial dysfunction is the key to CCH induced neurovascular injury: endothelial dysfunction, chronic neuroinflammation and myelination impairment.