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Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by an accumulation of lipid-derived reactive oxygen species （ROS）. The small-molecule compound erastin induces ferroptosis via inhibiting the cysteine-glutamate antiporter system, which consists of two subunits, namely the SLC7A11 and SLC3A2, respectively）. Recent studies have shown that SLC7A11 regulates ferroptosis in liver fibrosis, cardiomyopathy, and numerous other pathophysiological processes. The complex formed by SLC7A11 and SLC3A2 has also been suggested as a possible therapeutic target for cancer, as it is overexpressed in a wide variety of cancer types; moreover, inhibiting the system impairs cystine uptake, causing an accumulation of ROS and suppressing tumor growth. To counteract elevated levels of reactive oxygen species in cancerous cells system xc- is frequently upregulated, making it an attractive target for anticancer therapies. Overall, the SLC7A11 & SLC3A2 complex is a key player in multiple physiological processes and has significant potential as a therapeutic target for various diseases. The product of SLC7A11 & SLC3A2 complex may improve the development of its drug discovery.