Key result
Doxorubicin cardiotoxicity stems primarily from reactive oxygen species inducing oxidative stress and cardiomyocyte apoptosis.
Why the study?
Chemotherapy-induced cardiotoxicity is a significant complication with limited therapeutic options, and the role of gut microbiome alterations in this process is increasingly recognized but not fully understood.
Do microbiome-targeted therapies mitigate cardiovascular risk in cancer patients receiving chemotherapy?
Do microbiome-targeted therapies mitigate cardiovascular risk in cancer patients receiving chemotherapy?
Gut microbiome dysregulation, characterized by reduced SCFA and increased TMAO production, is a key mediator of chemotherapy-induced cardiotoxicity, highlighting microbiome-targeted therapies as a potential preventive strategy in cardio-oncology.
Dysbiosis with reduced SCFAs and elevated TMAO links to chemotherapy cardiotoxicity; supports microbiome interventions but leaves open need for clinical trials.
BACKGROUND: Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy, limiting treatment efficacy and worsening patient outcomes. Recent studies have implicated the gut microbiome and its key metabolites, such as short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO), in mediating inflammation, oxidative stress, and cardiac damage. The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction. AIM: To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients. Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Data extraction focused on microbiota alterations, mechanistic pathways, cardiac outcomes, and quality assessments using standardized risk-of-bias tools. RESULTS: Eighteen studies met the inclusion criteria. Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains. This imbalance contributed to gut barrier disruption, systemic inflammation, and oxidative stress, all of which promote myocardial damage. SCFA depletion weakened anti-inflammatory responses, while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction. Preclinical studies showed promising cardioprotective effects from probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, though human data remain limited. CONCLUSION: Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity. Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury. Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology, warranting further clinical validation through well-designed trials.
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Abdulaal et al. (2025) conducted a review in Chemotherapy-induced cardiotoxicity. Chemotherapy (specifically doxorubicin) was evaluated. Chemotherapy-induced cardiotoxicity, particularly from doxorubicin, is primarily mediated by the generation of reactive oxygen species leading to oxidative stress and cardiomyocyte apoptosis.
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