Key result
Review details the molecular mechanisms of cardiomyocyte death driving clinical drug-induced cardiotoxicity.
Why the study?
Drug-induced cardiotoxicity causes severe cardiac diseases and limits clinical use of implicated therapies, necessitating a theoretical basis and targets for prevention and treatment.
Understanding the diverse molecular mechanisms of cardiomyocyte death provides theoretical targets for preventing and treating drug-induced cardiotoxicity.
Homeostatic regulation of cardiomyocytes plays a crucial role in maintaining the normal physiological activity of cardiac tissue. Severe cardiotoxicity results in cardiac diseases including but not limited to arrhythmia, myocardial infarction and myocardial hypertrophy. Drug-induced cardiotoxicity limits or forbids further use of the implicated drugs. Such drugs that are currently available in the clinic include anti-tumor drugs (doxorubicin, cisplatin, trastuzumab, etc.), antidiabetic drugs (rosiglitazone and pioglitazone), and an antiviral drug (zidovudine). This review focused on cardiomyocyte death forms and related mechanisms underlying clinical drug-induced cardiotoxicity, including apoptosis, autophagy, necrosis, necroptosis, pryoptosis, and ferroptosis. The key proteins involved in cardiomyocyte death signaling were discussed and evaluated, aiming to provide a theoretical basis and target for the prevention and treatment of drug-induced cardiotoxicity in the clinical practice.
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Ma et al. (2020) conducted a review in Drug-induced cardiotoxicity. Cardiotoxic drugs (anti-tumor, antidiabetic, antiviral) was evaluated. This review summarizes the molecular mechanisms of cardiomyocyte death, including apoptosis, autophagy, necrosis, necroptosis, pyroptosis, and ferroptosis, in clinical drug-induced cardiotoxicity.
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