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Review
. 2020 Jun 3:8:434.
doi: 10.3389/fcell.2020.00434. eCollection 2020.

Molecular Mechanisms of Cardiomyocyte Death in Drug-Induced Cardiotoxicity

Wanjun Ma  1   2 , Shanshan Wei  1   2 , Bikui Zhang  1   2 , Wenqun Li  1   2
Affiliations
Review

Molecular Mechanisms of Cardiomyocyte Death in Drug-Induced Cardiotoxicity

Wanjun Ma et al. Front Cell Dev Biol. .

Abstract

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.

Keywords: apoptosis; autophagy; cardiomyocytes; cardiotoxicity; cell death; necrosis.

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Figures

FIGURE 1
FIGURE 1
Signaling pathways involved in drug-induced cardiotoxicity.
See this image and copyright information in PMC

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