ReviewInternational journal of general medicine2026
Mechanisms and the Role of p38 MAPK Signaling in Doxorubicin-Induced Cardiotoxicity: A Review.
Review in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
6 authors.
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Abstract
Doxorubicin (DOX) is a widely used anticancer agent, but its use carries the risk of cardiotoxicity. The underlying mechanisms of DOX-induced cardiac injury involve multiple interconnected processes, including oxidative stress, inflammatory activation, apoptosis, dysregulation of metal ion homeostasis, mitochondrial dysfunction, and impaired autophagy. The p38 mitogen-activated protein kinase (p38 MAPK) pathway functions as a stress-response central hub that integrates these signals and orchestrates downstream cellular outcomes via phosphorylation-dependent signaling cascades. This review summarizes current evidence on the molecular mechanisms of DOX-induced cardiotoxicity (DIC), with a focus on the pivotal role of the p38 MAPK pathway. We further discuss natural compounds that mitigate DIC via modulation of p38 MAPK signaling and examine emerging evidence on sex-specific cardioprotective effects mediated by distinct p38 MAPK isoforms. In addition, we briefly discuss the role of DOX nanoformulations in reducing cardiotoxicity, offering new insights into the mitigation of DIC.
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