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Acute kidney injury (AKI), often caused by ischemiareperfusion, results in the release of IL-1 and neutrophil-derived proteases into the circulation, directly impairing cardiomyocyte contractility and increasing arrhythmia susceptibility

Studies confirm that in the mouse heat stroke model, inhibiting p53 function via siRNA or p53 inhibitor (PFT-) can significantly reduce abnormal hepatocyte apoptosis in heat stress-induced ALI [51]

This triggers collagen synthesis , attracts immune cells, promotes blood vessel formation, and activates dozens of genes involved in tissue repair

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