The Therapeutic Potential of Stem Cell Therapy for Doxorubicin-Induced Cardiotoxicity: A Narrative Review.

Authors

Ali Mirzaei, Pouria Rezaei, Reza Golchin Vafa, Saleheh Jahani, Reza Arefnezhad, Hossein Fatemian, Mohammad Hossein Nikoo, Amirhossein Sahebkar, Fatemeh Rezaei-Tazangi

Published in

Health science reports. Volume 9. Issue 8. Pages e72924. Epub Jul 29, 2026.

Abstract

Doxorubicin (DOX) is a potent anthracycline chemotherapeutic agent whose clinical utility is significantly constrained by severe side effects, most notably DOX-induced cardiotoxicity (DIC). Pathophysiological mechanisms of DIC include oxidative stress, mitochondrial dysfunction, programmed cell death, and inflammation. Given the therapeutic potential of stem cell technology, this narrative review aims to summarize current evidence regarding the use of various stem cell types, particularly mesenchymal stem cells (MSCs), as a potential treatment for DIC.
This study conducted a comprehensive review of the literature concerning stem cell-based therapies in the context of DIC. We evaluated evidence regarding both pluripotent stem cells (including embryonic and induced pluripotent stem cells) and multipotent adult stem cells (such as bone marrow, adipose, and umbilical cord-derived MSCs) to assess their role in mitigating DOX-induced cardiac damage.
Current research indicates that stem cells, particularly MSCs, possess significant regenerative capabilities that may counteract the multifaceted pathophysiology of DIC. Evidence suggests that these cells can modulate inflammatory responses, alleviate oxidative stress, and support mitochondrial repair in damaged cardiac tissue, thereby offering a promising strategy to protect against or reverse chemotherapy-induced heart injury.
Stem cell-based therapy represents a promising and innovative frontier for the management of DOX-induced cardiotoxicity. While preclinical and emerging data highlight the therapeutic potential of MSCs in cardiac protection, further standardized research is required to fully elucidate their mechanisms and ensure clinical safety and efficacy for patients undergoing chemotherapy.

PMID:
42534466
Bibliographic data and abstract were imported from PubMed on 31 Jul 2026.

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