ReviewFrontiers in cardiovascular medicine2020
Angiotensin Converting Enzyme Inhibitors (ACEIs) Decrease the Progression of Cardiac Fibrosis in Rheumatic Heart Disease Through the Inhibition of IL-33/sST2.
Review in Frontiers in cardiovascular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03991910 (Randomised Controlled Trial Into the Role of Ramipril in Fibrosis Reduction in Rheumatic Heart Disease), which is not on this map. Cited by 26 papers.
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Randomised Controlled Trial Into the Role of Ramipril in Fibrosis Reduction in Rheumatic Heart Disease: The RamiRHeD Trial Protocol
Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Medical, interventional, and surgical management of rheumatic heart disease.Lancet regional health. Americas · 2026Review
- Valve biology and rheumatic heart disease pathogenesis.Nature cardiovascular research · 2026Review
- Article
- Upstream and Downstream Cardiovascular Changes in Rheumatic Mitral Stenosis: An Update.Journal of clinical medicine · 2025Review
- ACE inhibitors reduce the risk of myocardial fibrosis post-cardiac injury: a systematic review.The British journal of cardiology · 2025Article
- Interleukin family in vascular calcification: molecular mechanisms and therapeutic perspectives.Frontiers in cardiovascular medicine · 2025Review
- Expression profiles and bioinformatic analysis of circular RNA in rheumatic heart disease: potential hsa_circ_0001490 and hsa_circ_0001296 as a diagnostic biomarker.Frontiers in cardiovascular medicine · 2025Article
- Research on rheumatic heart disease from 2013 to early 2024: a bibliometric analysis.Journal of cardiothoracic surgery · 2024Article
- Review
- Sulfenylation of ERK1/2: A novel mechanism for SOHeliyon · 2024Article
- An Update on Mitral Valve Aging.Life (Basel, Switzerland) · 2024Review
- Angiotensin II and post-streptococcal glomerulonephritis.Clinical and experimental nephrology · 2024Review
- Review
- Clinical Outcome of Rheumatic Mitral Valve Repair and Replacement Surgery in Indonesia; A Comparison with Non-Rheumatic Aetiology.Global heart · 2024Article
- Roles of IL-33 in the Pathogenesis of Cardiac Disorders.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Global Left Ventricular Myocardial Work Efficiency in Patients With Severe Rheumatic Mitral Stenosis and Preserved Left Ventricular Ejection Fraction.Journal of cardiovascular imaging · 2023Article
- Distinct mononuclear diploid cardiac subpopulation with minimal cell-cell communications persists in embryonic and adult mammalian heart.Frontiers of medicine · 2023Article
- A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut.International journal of molecular sciences · 2023Review
- Topical captopril: a promising treatment for secondary lymphedema.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Myocardial fibrosis in rheumatic heart disease: emerging concepts and clinical implications.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatic heart disease (RHD) is common in developing countries and poses a big medical challenge and burden. The pathogenesis of RHD is influenced by the triad of host, agent, and environment. Autoantigens generated from Group A Streptococcus (GAS) infection are captured by the resident dendritic cells (DCs) in the heart's valvular endothelium. DCs differentiate into antigen presenting cells (APC) in the valve interstices. APC induces activation of autoreactive T cells, which triggers inflammation and tissue fibrosis. Cardiac fibrosis is promoted through the activation of Mitogen activated protein kinases (MAPKs) and its downstream signaling, including its interaction with transforming growth factor-β (TGF-β) and Smad proteins. TGF-β-induced phosphorylation of Smad2 complexes with Smad3 and Smad4, and translocates into the nucleus. Angiotensin II enhances the migration, maturation, and presentation of DC. In RHD, Angiotensin II induces fibrosis via the stimulation of TGF-β, which further increases the binding of IL-33 to sST2 but not ST2L, resulting in the upregulation of Angiotensin II and progression of cardiac fibrosis. This cascade of inflammation and valvular fibrosis causes calcification and stiffening of the heart valves in RHD. Angiotensin converting enzyme inhibitors (ACEIs) inhibit Angiotensin II production, which in turn decreases TGF-β expression and the onset of overt inflammatory response. This condition leads to a reduction in the sST2 as the decoy receptor to "steal" IL-33, and IL-33 binds to ST2L and results in cardioprotection against cardiac fibrosis in the pathogenesis of RHD.
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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 OpenQuestion graph.