Fig. 8 | Signal Transduction and Targeted Therapy

Fig. 8

From: Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion

Fig. 8

Schematic hypothesis. Cerebral ischemia leads to an unexpected increase in thrombin within neurons, promotes the mobilization of PE and PC in the phospholipid membrane of neuronal cells through cPLA2α, and accelerates the production of AA. Under the catalytic action of ACSL4, AA is esterified and made available as a ferroptotic fuel. This injury process can be blocked by thrombin inhibitors, cPLA2α inhibitors, and ACSL4 inhibitors. Concurrently, iron accumulates during I/R, which also contributes to ferroptosis and can be blocked by an iron chelator

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