ReviewCirculation research2016
The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.
Review in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 1,357 papers.
What it found
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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.
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
Phase 1 Feasibility and Safety of Whole Heart Radiotherapy for End-stage Heart Failure: First In-human Treatments
Who cites it
1,357 citing papers in PubMed.
- Mitochondria-derived peptide hydrogel augments mitochondrial transplantation for promoting cardiac repair via macrophage metabolic reprogramming.Bioactive materials · 2027Article
- A core-shell microneedle patch coordinates early anti-inflammatory modulation and sustained pro-angiogenic stimulation for cardiac repair after myocardial infarction.Materials today. Bio · 2026Article
- Targeted drug delivery systems for cardiovascular disease treatment: principles, targeting strategies, and future prospects.Annals of medicine · 2026Review
- Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026Review
- Beyond the Heart: Hepatic Extracellular Volume Assessment in Patients With Cardiovascular Disease.Journal of magnetic resonance imaging : JMRI · 2026Article
- Inflammatory cytokines and immune signalling in heart failure: mechanisms, models, and emerging therapies.Cardiovascular research · 2026Review
- Targeting the ENO1 metabolic checkpoint via microenvironment-responsive nanotherapeutics promotes postinfarction cardiac repair.Science advances · 2026Article
- Optimized cardiac leukocyte isolation for flow cytometry enumeration and sorting.American journal of physiology. Heart and circulatory physiology · 2026Article
- Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction.Basic research in cardiology · 2026Article
- Simultaneous 3-D Adiabatic TNMR in biomedicine · 2026Article
- A human two-hit platform modeling post-ischemic sterile inflammation and diastolic dysfunction in hiPSC-derived cardiac models.Materials today. Bio · 2026Article
- Timed metabolic repair after myocardial infarction.Nature cardiovascular research · 2026Article
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Short-chain fatty acids promote post-myocardial infarction cardiac repair via FFAR2-dependent suppression of osteoclast-like macrophage differentiation.Basic research in cardiology · 2026Article
- Article
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Collagen Prolyl 4-Hydroxylase: An Emerging Key Player in Cardiac Fibrosis.Journal of cardiovascular translational research · 2026Review
- A positively selected microRNA controls a reversible aging program in striated muscle.bioRxiv : the preprint server for biology · 2026Article
- NEAT1 Coordinates a PDLIM5-CACNA1C Regulatory Program Associated with a Potentially Arrhythmogenic Cardiomyocyte State in the Border Zone During Early Myocardial Infarction.International journal of molecular sciences · 2026Article
- Ellagic acid attenuates myocardial fibrosis by suppressing Bmi1-mediated inhibition of the p53/p21 pathway in cardiac fibroblasts.Molecular and cellular biochemistry · 2026Article
1,297 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.
Funding
Abstract
In adult mammals, massive sudden loss of cardiomyocytes after infarction overwhelms the limited regenerative capacity of the myocardium, resulting in the formation of a collagen-based scar. Necrotic cells release danger signals, activating innate immune pathways and triggering an intense inflammatory response. Stimulation of toll-like receptor signaling and complement activation induces expression of proinflammatory cytokines (such as interleukin-1 and tumor necrosis factor-α) and chemokines (such as monocyte chemoattractant protein-1/ chemokine (C-C motif) ligand 2 [CCL2]). Inflammatory signals promote adhesive interactions between leukocytes and endothelial cells, leading to extravasation of neutrophils and monocytes. As infiltrating leukocytes clear the infarct from dead cells, mediators repressing inflammation are released, and anti-inflammatory mononuclear cell subsets predominate. Suppression of the inflammatory response is associated with activation of reparative cells. Fibroblasts proliferate, undergo myofibroblast transdifferentiation, and deposit large amounts of extracellular matrix proteins maintaining the structural integrity of the infarcted ventricle. The renin-angiotensin-aldosterone system and members of the transforming growth factor-β family play an important role in activation of infarct myofibroblasts. Maturation of the scar follows, as a network of cross-linked collagenous matrix is formed and granulation tissue cells become apoptotic. This review discusses the cellular effectors and molecular signals regulating the inflammatory and reparative response after myocardial infarction. Dysregulation of immune pathways, impaired suppression of postinfarction inflammation, perturbed spatial containment of the inflammatory response, and overactive fibrosis may cause adverse remodeling in patients with infarction contributing to the pathogenesis of heart failure. Therapeutic modulation of the inflammatory and reparative response may hold promise for the prevention of postinfarction 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.