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. 2022 Sep 13;23(18):10617. doi: 10.3390/ijms231810617

Figure 2.

Figure 2

Mechanisms of non-anthracycline-based chemotherapeutic cardiotoxicity. The mechanisms of cisplatin toxicity to the heart include oxidative stress, inflammation, endoplasmic reticulum stress, and activation of ERK1/2 and p38 MAPK pathways. Cyclophosphamide causes myocardial injury mainly by inducing oxidative stress, nitrative stress, and inhibiting the PI3K/AKT/mTOR pathway. MTX activates proinflammatory pathways, inhibits Bcl2 expression, and induces cardiomyocyte apoptosis. 5-FU activates mitophagy and blocks the TCA cycle, thereby causing mitochondrial dysfunction. CYCL, cyclophosphamide; PLA, platinum; vWF, von Willebrand factor; t-PA, tissue plasminogen activator; hs-CRP, high-sensitivity C-reactive protein, PAI-1, plasminogen activator inhibitor; NF-κB, nuclear factor kappa B; eNOS, endothelial nitric oxide synthase; Keap1, Kelch-like ECH-associated protein 1; Nrf2, nuclear factor erythroid 2-related factor 2. Created with BioRender.com.