ReviewMolecular biology reports2026
Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.
Review in Molecular biology reports, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Authors and funding
6 authors.
Funding
Abstract
Rheumatic heart disease (RHD) is a chronic, immune-mediated valvular disorder triggered by Group A β-hemolytic streptococcal infection. Persistent inflammation and immune-mediated tissue injury are central features of disease progression, whereas the roles of hormonal and metabolic regulatory pathways remain less well defined. Emerging evidence suggests that inflammatory signaling may intersect with hormonal and metabolic pathways during the transition from rheumatic fever to chronic valvular disease. Pro-inflammatory mediators have been associated with immune activation and extracellular matrix remodeling, with potential involvement of pathways such as nuclear factor-κB, Janus kinase/signal transducer and activator of transcription, and the NOD-like receptor protein 3 inflammasome. Chronic inflammation may also be accompanied by altered neuroendocrine anti-inflammatory feedback, including changes in glucocorticoid receptor signaling and hypothalamic-pituitary-adrenal axis regulation. In addition, sex hormones, thyroid hormones, and metabolic hormones may be linked to immune-cell differentiation, endothelial function, and valvular cell phenotypes, suggesting a possible inflammatory-endocrine regulatory loop that remains insufficiently validated in RHD-specific studies. These relationships may provide a context for understanding valvular interstitial cell activation, endothelial dysfunction, endothelial-mesenchymal transition, metabolic reprogramming, energy imbalance, fibrosis, and calcification, but direct causal evidence remains limited. Future dual-target strategies addressing both inflammatory and hormonal signaling may provide a theoretical framework for individualized intervention; however, their efficacy and safety require rigorous RHD-specific validation. This review summarizes current evidence and discusses the inflammatory-hormonal network as a hypothesis-generating framework for understanding chronic rheumatic valvular remodeling.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.