ReviewInternational journal of biological sciences2018
Cardiac fibrosis: new insights into the pathogenesis.
Review in International journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05335629 (Evaluation of the Effect of Dapagliflozin on Cardiac Remodeling in Post Myocardial Infarction Patients), which is not on this map. Cited by 189 papers, 2 of them syntheses that pooled it.
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.
Evaluation of the Effect of Dapagliflozin on Cardiac Remodeling in Post Myocardial Infarction Patients
Who cites it
189 citing papers in PubMed, 2 syntheses or guidelines pooled it, 325 citations in OpenAlex.
- Pooled it
- A Systematic Review of the Biological Effects of Cordycepin.Molecules (Basel, Switzerland) · 2021Pooled it
- ADAMTS4 mediates LPS-induced cardiac injury and myocardial fibrosis through proteolytic cleavage of TSP1.Clinical and translational medicine · 2026Article
- Role of (pro) renin receptor in adriamycin-induced cardiomyopathy.International journal of cardiology. Heart & vasculature · 2026Article
- Myocardial fibrosis and viability: the role of imaging and biomarkers in patients with chronic total occlusion on coronary angiography.Biochemia medica · 2026Review
- Oxygen Transport Impairment in the Failing Heart: A Histology-Image-Based Computational Analysis.Annals of biomedical engineering · 2026Article
- The heart's fibrous web: A bibliometric analysis of cardiac fibrosis in Asia and Oceania.Medicine · 2026Article
- Small-molecule LF3 alleviates angiotensin II-induced cardiac dysfunction via attenuating cardiac fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Identification of biomarkers in myocardial hypertrophy and fibrosis via integrated transcriptomic and phosphoproteomic profiling.Scientific reports · 2026Article
- Stable and functional regulatory T cell attenuates fibrotic remodeling in heart failure.Regenerative therapy · 2026Article
- Review
- Lipopolysaccharide-induced histone lactylation mediates m6A RNA modification causing mitochondrial dysfunction and pulmonary fibroblasts activation to exacerbate sepsis-associated pulmonary fibrosis.Respiratory research · 2025Article
- ER stress inhibitor 4PBA attenuates hindlimb unloading-induced cardiac mitochondrial and metabolic dysfunction.Pflugers Archiv : European journal of physiology · 2025Article
- A Molecular Perspective on the Intricate Interplay Among Exosomes, Bioenergetic Metabolism, and the Pathogenesis of Diabetic Cardiomyopathy.Journal of cardiovascular translational research · 2025Review
- Decoding the impact of gut microbiota on heart failure.Genes & diseases · 2025Review
- Septin4 Regulates Cardiac Fibrosis After Pressure Overload.Circulation research · 2025Article
- Adrenomedullin production by adult cardiac fibroblasts via NF-κB/STAT6 signaling enhances post-infarction lymphangiogenesis and cardiac repair.Scientific reports · 2025Article
- Pharmacological inhibition of apoptosis, necroptosis, and ferroptosis confers effective cardioprotection in post-myocardial infarction in rats.Scientific reports · 2025Article
- Revolutionizing cardiac fibrosis treatment: the potential of personalized CAR T-cell therapy.Cardio-oncology (London, England) · 2025Review
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
129 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis is defined as the imbalance of extracellular matrix (ECM) production and degradation, thus contributing to cardiac dysfunction in many cardiac pathophysiologic conditions. This review discusses specific markers and origin of cardiac fibroblasts (CFs), and the underlying mechanism involved in the development of cardiac fibrosis. Currently, there are no CFs-specific molecular markers. Most studies use co-labelling with panels of antibodies that can recognize CFs. Origin of fibroblasts is heterogeneous. After fibrotic stimuli, the levels of myocardial pro-fibrotic growth factors and cytokines are increased. These pro-fibrotic growth factors and cytokines bind to its receptors and then trigger the activation of signaling pathway and transcriptional factors via Smad-dependent or Smad independent-manners. These fibrosis-related transcriptional factors regulate gene expression that are involved in the fibrosis to amplify the fibrotic response. Understanding the mechanisms responsible for initiation, progression, and amplification of cardiac fibrosis are of great clinical significance to find drugs that can prevent the progression of cardiac fibrosis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.