ReviewCell and tissue research2016
Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration.
Review in Cell and tissue research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05531955 (A Study of Pirfenidone in the Treatment of Myocardial Fibrosis After Acute Myocardial Infarction), which is not on this map. Cited by 494 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.
A Study of Pirfenidone in the Treatment of Myocardial Fibrosis After Acute Myocardial Infarction: a Phase II Prospective, Randomized, Double-blind，Placebo Controlled Clinical Trial
Who cites it
494 citing papers in PubMed, 872 citations in OpenAlex.
- Efficacy and safety of levosimendan in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention: The LEVOCEST trial.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2024Trial
- Multi-modality deep learning-based [European journal of nuclear medicine and molecular imaging · 2024Trial
- Click chemistry-modified cardiomyocytes enhance cardiac contractility and prevent remodeling in ischemia-reperfusion injured hearts.Bioactive materials · 2027Article
- Early post-infarct fibroblast activation protein-targeted PET/CT withEuropean journal of nuclear medicine and molecular imaging · 2026Article
- Gfpt2 modulates fibroblast activation by glutathione metabolism.Journal of molecular and cellular cardiology · 2026Article
- MiR-145-5p modulates collagen production and fibroblast behaviour after cardiac injury partially via COL5A1.Basic research in cardiology · 2026Article
- Article
- An integrated overview of acute heart failure: a narrative review of pathophysiological mechanisms and contributing factors.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026Review
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Human pericardial macrophages suppress cardiac fibrosis through cystatin C signaling after myocardial infarction.JCI insight · 2026Article
- Collagen Prolyl 4-Hydroxylase: An Emerging Key Player in Cardiac Fibrosis.Journal of cardiovascular translational research · 2026Review
- Post-MI Remodeling Mechanics of Left Ventricle: Microstructure-Informed Models, Identifiability, and Uncertainty for Patient-Specific Prediction.Bioengineering (Basel, Switzerland) · 2026Review
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- The Role of the Extracellular Volume of the Infarction Zone and the Remote Myocardium in Predicting Systolic Dysfunction After the First Myocardial Infarction.Diagnostics (Basel, Switzerland) · 2026Article
- Molecular mechanisms, therapeutic strategies, and inter-organ fibrosis crosstalk of Gla proteins in cardiovascular disease.Communications biology · 2026Review
- Cardiac regeneration and repair: the emerging mechanisms and therapeutic approaches.Molecular biomedicine · 2026Review
- Slick K+ channels contribute to cardiac remodeling, fibrosis, and dysfunction in postinfarction hearts.JCI insight · 2026Article
- S100A9 Aggravates Cardiac Fibrosis by TLR4/PGC-1α Mediated Macrophage-Myofibroblast Crosstalk.Journal of extracellular vesicles · 2026Article
- Primary cilia promote cardiac fibrosis and limit heart function after myocardial infarction.bioRxiv : the preprint server for biology · 2026Article
- Ellagic Acid Attenuates Oxidative Stress and Improves Cardiovascular Function Following Myocardial Infarction in Ovariectomized Rats.Journal of cellular and molecular medicine · 2026Article
434 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic cell death during a myocardial infarction leads to a multiphase reparative response in which the damaged tissue is replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. This also induces geometrical, biomechanical, and biochemical changes in the uninjured ventricular wall eliciting a reactive remodeling process that includes interstitial and perivascular fibrosis. Although the initial reparative fibrosis is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental as they lead to progressive impairment of cardiac function and eventually to heart failure. In this review, we summarize current knowledge of the mechanisms of both reparative and reactive cardiac fibrosis in response to myocardial infarction, discuss the potential of inducing cardiac regeneration through direct reprogramming of fibroblasts and myofibroblasts into cardiomyocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis. Graphical abstract Reparative response following a myocardial infarction. Hypoxia-induced cardiomyocyte death leads to the activation of myofibroblasts and a reparative fibrotic response in the injured area. Right top In adult mammals, the fibrotic scar formed at the infarcted area is permanent and promotes reactive fibrosis in the uninjured myocardium. Right bottom In teleost fish and newts and in embryonic and neonatal mammals, the initial formation of a fibrotic scar is followed by regeneration of the cardiac muscle tissue. Induction of post-infarction cardiac regeneration in adult mammals is currently the target of intensive research and drug discovery attempts.
Indexed as
Identifiers
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.