Specific Intestinal Fungi Play Role in the Pathogenesis of MASLD and Cardiovascular Disease

Why It Matters

By connecting gut fungal composition to subclinical atherosclerosis, the research opens new pathways for early cardiovascular screening and targeted therapies in patients with advanced liver disease.

Key Takeaways

• Candida albicans abundance higher in MASLD patients with cirrhosis
• C. albicans levels correlate with coronary artery calcification scores
• CAC linked to liver stiffness measured by MRE, not fat fraction
• Age, diabetes, obesity, cirrhosis, C. albicans predict CAC ≥100 AU
• Findings suggest gut mycobiome as potential CVD biomarker in MASLD

Pulse Analysis

Metabolic dysfunction‑associated steatotic liver disease (MASLD) has emerged as a leading cause of chronic liver injury and a recognized accelerator of cardiovascular disease (CVD). While the bacterial gut microbiome has been extensively mapped for its role in metabolic inflammation, the mycobiome—particularly opportunistic yeasts such as Candida—has received far less attention. Recent advances in sequencing technologies now allow researchers to profile fungal communities with the same resolution as bacterial taxa, revealing that dysbiosis of the gut mycobiome may be an underappreciated driver of systemic vascular pathology.

The cross‑sectional analysis of 103 MASLD patients demonstrated a robust association between fecal Candida albicans abundance and coronary artery calcification (CAC), a gold‑standard surrogate for subclinical atherosclerosis. Notably, CAC correlated strongly with liver stiffness measured by magnetic resonance elastography, suggesting that fibrotic remodeling, rather than simple steatosis, amplifies cardiovascular risk. Multivariate modeling confirmed that age, diabetes, obesity, cirrhosis and enriched C. albicans independently predicted CAC scores of 100 Agatston units or higher, implicating fungal‑driven inflammation—potentially via interleukin‑6 and tumor necrosis factor‑α pathways—as a mechanistic link.

These findings position the gut mycobiome as a promising biomarker suite for early CVD detection in MASLD, offering a non‑invasive complement to imaging and serum tests. Clinicians could eventually integrate fecal fungal profiling into risk algorithms, while researchers explore antifungal or microbiome‑modulating interventions to blunt the atherogenic cascade. However, longitudinal studies are needed to confirm causality and to determine whether modifying Candida load translates into reduced coronary calcification or clinical events. If validated, such strategies could usher in personalized, microbiome‑guided therapies for the intertwined epidemics of liver disease and cardiovascular morbidity.