Understanding MASLD — from molecular pathogenesis to cardiovascular risk: A concise review for the clinical cardiologist

Aug 28, 2025Atherosclerosis

MASLD: From Molecular Causes to Heart Disease Risk – A Brief Guide for Heart Doctors

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Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with increased risk of cardiovascular disease outcomes, including heart failure and myocardial infarction.

MASLD is linked to a higher likelihood of coronary artery disease, stroke, and atrial fibrillation.
Shared mechanisms such as insulin resistance and chronic inflammation contribute to both liver and heart issues.
The stage of fibrosis in the liver, which is a key indicator of liver health, also relates to cardiovascular risks but is often overlooked in current assessments.
Non-invasive markers for liver fibrosis, like FIB-4 and elastography, are being recognized as useful for evaluating cardiovascular risk.
Certain medications, including GLP-1 receptor agonists and SGLT2 inhibitors, may improve both liver and heart health.

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BACKGROUND AND AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently replaced non-alcoholic fatty liver disease (NAFLD) as the preferred nomenclature, reflecting a shift toward inclusion-based diagnostic criteria rooted in metabolic dysfunction. Beyond its hepatic implications, MASLD has emerged as an independent, modifiable driver of cardiovascular disease (CVD).

METHODS: This review summarizes and synthesizes robust epidemiological and mechanistic evidence linking MASLD to cardiovascular outcomes.

RESULTS: MASLD is associated with increased risk of coronary artery disease, myocardial infarction, atrial fibrillation, stroke, and heart failure-particularly heart failure with preserved ejection fraction (HFpEF). Shared pathophysiological mechanisms include insulin resistance, chronic inflammation, oxidative stress, endothelial dysfunction, and atherogenic dyslipidemia, which collectively contribute to both hepatic fibrogenesis and vascular injury. Fibrosis stage, the strongest predictor of hepatic outcomes, also correlates with subclinical atherosclerosis and cardiovascular mortality, yet remains unaccounted for in current CVD risk models. Non-invasive fibrosis markers such as FIB-4 and elastography, originally developed for hepatology, are gaining traction in cardiovascular risk stratification. Furthermore, pharmacologic agents such as GLP-1 receptor agonists and SGLT2 inhibitors demonstrate dual efficacy in improving hepatic, metabolic, and cardiovascular outcomes.

CONCLUSIONS: This review provides an updated synthesis for cardiologists, outlining the evolution of MASLD nomenclature, its systemic pathophysiology, and its clinical implications-underscoring the urgent need for integrated, multidisciplinary management of this underrecognized cardiometabolic disease.

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Understanding MASLD — from molecular pathogenesis to cardiovascular risk: A concise review for the clinical cardiologist

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