Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies

The therapeutic prowess of doxorubicin in oncology is marred by its cardiotoxic consequences, manifesting as cardiac remodeling. Pathophysiological alterations triggered by doxorubicin include inflammatory cascades, fibrotic tissue deposition, vascular and valvular changes, and finally cardiomyopathy. These multifarious consequences collectively orchestrate the deterioration of cardiac architecture and function.

By charting the molecular underpinnings and remedial prospects, this review aspires to contribute a novel perspective using latest publications to the ongoing quest for cardioprotection in cancer therapy.

Experimental analyses demonstrate the pivotal roles of oxidative stress and subsequent necrosis and apoptosis of cardiomyocytes, muscle cells, endothelial cells, and small muscle cells in different parts of the heart. In addition, severe and unusual infiltration of macrophages, mast cells, and neutrophils can amplify oxidative damage and subsequent impacts such as chronic inflammatory responses, vascular and valvular remodeling, and fibrosis. These modifications can render cardiomyopathy, ischemia, heart attack, and other disorders. In an endeavor to counteract these ramifications, a spectrum of emerging adjuvants and strategies are poised to fortify the heart against doxorubicin's deleterious effects.

The compendium of mitigation tactics such as innovative pharmacological agents hold the potential to attenuate the cardiotoxic burden.