ReviewFrontiers in endocrinology2026
Endocrine regulation of cardiac fibrosis: implications for HFpEF.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Heart failure with preserved ejection fraction (HFpEF) is a dominant heart failure phenotype in ageing populations and commonly develops on a background of hypertension, obesity, diabetes, and systemic inflammation. Myocardial fibrosis is a central structural lesion in HFpEF, but it is increasingly recognised not merely as a passive haemodynamic consequence but as an actively regulated process shaped by endocrine and metabolic signals. This review examines seven interacting hormonal axes, namely the renin-angiotensin-aldosterone system, tissue-amplified glucocorticoid signalling via 11β-HSD1, gonadal steroid deficiency, adipokine dysregulation and epicardial adipose tissue inflammation, insulin resistance, altered thyroid hormone signalling, and disordered mineral metabolism, which converge on shared profibrotic effectors, including TGF-β-Smad signalling, NADPH oxidase-derived oxidative stress, suppression of the NO-cGMP-PKG pathway, and mTOR-AMPK-FOXO dysregulation. These axes interact via self-reinforcing feedback circuits and converge on coronary microvascular dysfunction as a central pathological node, helping to explain the heterogeneity of HFpEF, its female predominance, and incomplete responses to single-pathway therapies. We distinguish clinically validated endocrine-modulating strategies, including SGLT2 inhibitors, mineralocorticoid receptor antagonism, and incretin-based therapy in selected phenotypes, from emerging tissue-targeted approaches. This endocrine framework provides a basis for phenotype-guided antifibrotic strategies in HFpEF.
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