ReviewCellular signalling2021
The role of Smad signaling cascades in cardiac fibrosis.
Review in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 123 citations in OpenAlex.
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Galectin-3, transforming growth factor beta 1, and brain natriuretic peptide in cardiac remodeling under hyperlipidemic and hyperglycemic stress.Molecular and cellular biochemistry · 2026Article
- Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.Molecular biology reports · 2026Review
- "Comprehensive multi-omics of age-respective plasma and matrix-bound extracellular vesicles identifies anti-fibrotic miRNAs validated on a heart-on-a-chip".Biomaterials · 2026Article
- Cell migration inducing protein alleviates adverse cardiac remodelling after ischaemia and reperfusion injury by controlling fibroblast activation.Cardiovascular research · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Narrative review of fluid dynamics in the left ventricle: from the perspective of aortic regurgitation.Journal of thoracic disease · 2026Review
- Cardioprotective Role of CalhexCell biochemistry and biophysics · 2026Review
- Study on the Antioxidant and Anti-Myocardial Fibrosis Effects of a Phenylpropanoid Compound (Xanthiumnolic C) Derived fromACS omega · 2026Article
- Hyperbaric Oxygen Therapy in Experimental Autoimmune Myocarditis: Insights from Preclinical Models to Translational Perspectives.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Myocardial Matrix Metalloproteinase 3 Protein Expression in Ischemic Heart Failure.International journal of molecular sciences · 2026Article
- The role of different types of programmed cell death in myocardial fibrosis: from mechanisms to therapeutics.Frontiers in cardiovascular medicine · 2026Review
- Beyond cardiac fibroblasts: research advances on understanding and targeting intercellular communication networks in cardiac fibrosis.Frontiers in cardiovascular medicine · 2026Review
- Orchestrating HFpEF: How Noncoding RNAs Drive Pathophysiology and Phenotypic Outcomes.International journal of molecular sciences · 2025Review
- Epigallocatechin Gallate as a Molecular Therapeutic in Heart Failure and Cardio-Oncology: Mechanistic Pathways and Translational Perspectives.International journal of molecular sciences · 2025Review
- Association between serum uric acid and prostate cancer risk: The modifying role ofJournal of clinical and translational research · 2025Article
- Coordinated expression of BMP10/ALK1/endoglin-proteins that drive embryonic cardiac and vascular morphogenesis-in patients with heart failure: The EMPEROR Program.European journal of heart failure · 2025Article
- Revolutionizing cardiac fibrosis treatment: the potential of personalized CAR T-cell therapy.Cardio-oncology (London, England) · 2025Review
- Novel high throughput 3D ECM remodeling assay identifies MEK as key driver of fibrotic fibroblast activity.Materials today. Bio · 2025Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Most myocardial pathologic conditions are associated with cardiac fibrosis, the expansion of the cardiac interstitium through deposition of extracellular matrix (ECM) proteins. Although replacement fibrosis plays a reparative role after myocardial infarction, excessive, unrestrained or dysregulated myocardial ECM deposition is associated with ventricular dysfunction, dysrhythmias and adverse prognosis in patients with heart failure. The members of the Transforming Growth Factor (TGF)-β superfamily are critical regulators of cardiac repair, remodeling and fibrosis. TGF-βs are released and activated in injured tissues, bind to their receptors and transduce signals in part through activation of cascades involving a family of intracellular effectors the receptor-activated Smads (R-Smads). This review manuscript summarizes our knowledge on the role of Smad signaling cascades in cardiac fibrosis. Smad3, the best-characterized member of the family plays a critical role in activation of a myofibroblast phenotype, stimulation of ECM synthesis, integrin expression and secretion of proteases and anti-proteases. In vivo, fibroblast Smad3 signaling is critically involved in scar organization and exerts matrix-preserving actions. Although Smad2 also regulates fibroblast function in vitro, its in vivo role in rodent models of cardiac fibrosis seems more limited. Very limited information is available on the potential involvement of the Smad1/5/8 cascade in cardiac fibrosis. Dissection of the cellular actions of Smads in cardiac fibrosis, and identification of patient subsets with overactive or dysregulated myocardial Smad-dependent fibrogenic responses are critical for design of successful therapeutic strategies in patients with fibrosis-associated heart failure.
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What OpenQuestion holds
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 OpenQuestion graph.