The role of IL-6 in hypertrophic and dilated cardiomyopathy: clinical and therapeutic implications.

Authors

Lydia Krexi, Dimitra Krexi, Timothy Rider Betts

Published in

Heart failure reviews. Volume 31. Issue 1. Aug 10, 2026. Epub Aug 10, 2026.

Abstract

Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are genetically heterogeneous myocardial disorders in which disease progression is influenced by secondary modifiers beyond structural gene mutations. Increasing evidence suggests that inflammatory signalling plays a role in modulating disease phenotype and progression. Among inflammatory mediators, interleukin-6 (IL-6) has emerged as a potential contributor to myocardial remodelling and dysfunction.A structured literature review was performed using Ovid MEDLINE and the Cochrane Library for studies published up to 10 October 2025. Findings were synthesised narratively because of substantial heterogeneity in study design, populations, and outcomes.This review synthesises clinical, genetic, and experimental evidence on the role of IL-6 in HCM and DCM, with a focus on its potential therapeutic relevance. Across studies, elevated IL-6 levels are consistently associated with greater disease severity. Mechanistic data indicate that IL-6 signalling via the gp130/STAT3 pathway may promote cardiomyocyte hypertrophy, fibrosis, and apoptosis, with genetic polymorphisms likely influencing disease susceptibility and phenotypic expression. Pharmacological interventions with anti-inflammatory properties, including statins, pentoxifylline, and growth hormone, have been associated with reductions in IL-6 levels and improvements in cardiac function, although these effects are not specific to IL-6 signalling.In summary, current evidence supports IL-6 as an important component of the inflammatory milieu associated with HCM and DCM and suggests potential utility as a biomarker of disease activity. However, evidence supporting a causal pathogenic role remains limited, and IL-6-directed therapies have not been systematically evaluated in cardiomyopathy populations.

PMID:
42572064
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.

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