Regulation of mammalian target of rapamycin on ferroptosis: from mechanism to therapeutics in septic cardiomyopathy

Whether it is activating the adenosine monophosphate-activated protein kinase (AMPK)–mTOR pathway to improve autophagy level, or enhancing autophagy flux, it can significantly promote the occurrence of ferroptosis. [...]in the SIC model, the latest evidence demonstrated that lipopolysaccharide (LPS) increased the expression of nuclear receptor coactivator 4, which aggravated ferritinophagy-mediated ferroptosis. [...]selective mTOR inhibitor can reportedly induce the expression of eukaryotic initiation factor eIF4E-binding proteins downstream of mTOR and decrease GPx4 protein levels leading to accelerated ferroptosis. In the absence of glucose, AMPK can be activated to initiate an energy stress protection program to counter ferroptosis by disrupting the biosynthesis of PUFAs. [...]variations in mTOR expression levels can reportedly affect the activity of the AMPK pathway. [...]an in-depth analysis of mTOR regulation on ferroptosis is essential to deeply understand the pathogenesis of SIC and provide new horizons for clinical diagnosis and treatment.