ArticleCellular signalling2021
Cardiac fibrosis: Pathobiology and therapeutic targets.
Article in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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Who cites it
43 citing papers in PubMed.
- Collagen Prolyl 4-Hydroxylase: An Emerging Key Player in Cardiac Fibrosis.Journal of cardiovascular translational research · 2026Review
- Role of ATOH8 in Mitigating Cardiac Fibrosis in Heart Failure via Inhibition of the Transcriptional Repression of Smad7 by RUNX2.Biomolecules & therapeutics · 2026Article
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Challenges and opportunities for ginseng-based medicines in treating cardiac fibrosis from mechanistic insights to clinical translation.Chinese herbal medicines · 2026Review
- Bioinformatics Identification and Molecular Docking Validation of Post-Translational Modification-Related Hub Genes as Diagnostic Biomarkers and Therapeutic Targets in Myocardial Fibrosis.International journal of molecular sciences · 2026Article
- Antibody-conjugated SIS3-loaded PLGA@polydopamine nanoparticles alleviate cardiac fibrosis by modulating Smad3 signaling in myofibroblasts.Journal of nanobiotechnology · 2026Article
- Serpine1 Regulates the Enhanced Inhibitory Effect of CHIR99021 Combined with Fibroblast Growth Factor 2 on Myocardial Fibrosis After Myocardial Infarction in Mice.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
- The TREM2 paradox in fibrosis: a unified mechanism for opposite outcomes across organs.Frontiers in immunology · 2026Review
- Obesity-Associated Cardiac Fibrosis: Mechanisms and Emerging Therapeutic Targets.Vascular health and risk management · 2026Review
- Meox1 Promotes Cardiac Fibrosis and Pathological Remodeling following Myocardial Infarction through Cthrc1/p-Smad2/3 Signaling.International journal of biological sciences · 2026Article
- Mixed short-chain fatty acids and high-fiber diet reshape SCFA profiles and attenuate post-infarction cardiac fibrosis in mice.Frontiers in cardiovascular medicine · 2026Article
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Hypoxia-preconditioned MiotEVs from bone marrow mesenchymal stem cells inhibit myocardial infarction-induced cardiac fibrosis.Bioengineering & translational medicine · 2026Article
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- Zhilong Huoxue Tongyu capsule inhibits hypertensive myocardial fibrosis via balancing TGF-β1/Smad3/Erbb4-IR/miR-29b pathway.Scientific reports · 2025Article
- Cardiac structural and molecular alterations in rodent models of temporal lobe epilepsy.Epilepsia open · 2025Article
- Decoding the regulatory roles of circular RNAs in cardiac fibrosis.Non-coding RNA research · 2025Review
- The Role of Signalling Pathways in Myocardial Fibrosis in Hypertrophic Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- Effects of bisoprolol combined with torasemide on cardiac electrophysiology in patients with acute myocardial infarction and heart failure.Frontiers in physiology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Cardiac fibrosis is characteristic of the end stage in nearly all forms of heart disease. Accumulation of extracellular matrix in the myocardium leads to increased risk of arrhythmia and impaired cardiac function, and ultimately progression to heart failure. Despite the critical need to slow or reverse development of cardiac fibrosis to maintain cardiac function, there are no approved therapies that directly target the extracellular matrix. Research into the underlying causes and therapeutic targets has been hampered, in part, by the lack of a clear marker for cardiac fibroblasts - the cells responsible for regulating extracellular matrix turnover. Lineage tracing studies as well as single-cell RNA sequencing studies have provided new insights into cardiac fibroblast origins and heterogeneity. Moreover, a greater understanding of pathways governing fibroblast activation during ischemic and non-ischemic cardiac remodeling and their communication with other inflammatory and cardiac cells may lead to novel therapeutic targets to slow or reverse fibrotic remodeling. The special issue of Cellular Signaling entitled "Cardiac Fibrosis: Pathobiology and Therapeutic Targets" is comprised of review articles in which these topics, as well as important open questions for future investigation, are discussed.
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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 OpenQuestion graph.