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There is significant evidence that, besides inducing overexpression of the genetic expression and an increase in apoptosis inhibitory proteins (Bcl-2, Bcl-xL, XiAP), IL-8 can also inhibit proteolytic activation of caspase-3

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another beneficial effect of HGF following myocardial infarction could lie in its ability to induce neovascularization, which could support formation of new cardiac vasculature that would improve reperfusion of the myocardium

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In addition, ATV ameliorated ferroptosis-dependent myocardial injury and inflammation following CME by inhibiting the Hif1a/Ptgs2 pathway