Key result
MASLD acts as a potentially modifiable amplifier of cancer therapy-related cardiovascular toxicity.
Why the study?
MASLD may act as a potential amplifier of cancer therapy-related cardiovascular toxicity, raising the question of whether lifestyle and dietary interventions can mitigate this cumulative risk.
MASLD may act as a systemic amplifier of cancer therapy-related cardiovascular toxicity, suggesting that hepatic phenotyping and personalized nutrition should be integrated into cardio-oncology risk stratification.
Hypothesis-generating for MASLD-amplified cardiotoxicity; prospective trials needed before hepatic phenotyping or nutrition alters cardio-oncology practice.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent worldwide and represents the hepatic manifestation of a systemic cardiometabolic-inflammatory syndrome rather than an isolated organ disease. In parallel, anticancer therapies carry a well-recognised burden of cancer therapy-related cardiovascular toxicity (CTR-CVT). Evidence suggests that the metabolic-inflammatory cascade driving steatosis → steatohepatitis → fibrosis may also contribute to endothelial dysfunction, myocardial remodelling and cardiomyocyte vulnerability to chemotherapy-induced oxidative stress. This narrative review proposes a unifying conceptual framework in which MASLD may act as a potential amplifier of cardiotoxicity in oncology patients and examines whether lifestyle and dietary interventions could mitigate this cumulative risk. Methods: A structured literature search of PubMed, Scopus and Web of Science was performed, prioritising systematic reviews, meta-analyses, randomised controlled trials, large cohort studies and recent international guidelines on MASLD, cardio-oncology and nutritional interventions. Results: Four converging molecular axes were identified as plausible links between MASLD and cardiomyocyte susceptibility to anticancer therapy: mitochondrial dysfunction with reactive oxygen species overproduction, NLRP3 inflammasome activation and metaflammation, endothelial nitric oxide impairment, and pro-fibrotic TGF-β/hepatic stellate cell signalling. Mediterranean-style dietary patterns, selected micronutrients and emerging metabolic therapies modulate the same network and may offer translational opportunities. Conclusions: Reframing MASLD as a potentially modifiable amplifier of CTR-CVT supports the integration of hepatic phenotyping into baseline cardio-oncology risk stratification and the use of personalised nutrition as a precision tool acting on shared mitochondrial, inflammatory, endothelial and fibrotic pathways. Multidisciplinary framework and prospective interventional studies, adopting composite hepato-cardio-oncological endpoints, are warranted.
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Rocca et al. (2026) conducted a review in Metabolic dysfunction-associated steatotic liver disease (MASLD) and cancer therapy-related cardiovascular toxicity (CTR-CVT). Personalized nutrition and lifestyle interventions was evaluated. Metabolic dysfunction-associated steatotic liver disease (MASLD) acts as a potentially modifiable amplifier of cancer therapy-related cardiovascular toxicity, which may be mitigated by personalized nutrition and hepatic phenotyping.
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