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Tumor necrosis factor-alpha-induced targeted proteolysis of cystathionine beta-synthase modulates redox homeostasis

Support for GHK-Cus systemic effects is based principally on animal and in vitro studies, but the findings give reason to be optimistic about its potential as an injectable treatment

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Furthermore, advanced research into ferroptosis mechanisms in CHD may identify novel targets and strategies for CHD prevention and treatment, potentially mitigating myocardial injury by inhibiting ferroptosis-related signaling pathways or enhancing antioxidant capacity, ultimately improving cardiac function and quality of life for CHD patients

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