ReviewPharmacology & therapeutics2018
Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.
Review in Pharmacology & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 519 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
519 citing papers in PubMed, 2 syntheses or guidelines pooled it, 916 citations in OpenAlex.
- Colchicine in Patients With Recent Myocardial Infarction: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Journal of the American Heart Association · 2026Pooled it
- Hydroxysafflor yellow A for ischemic heart diseases: a systematic review and meta-analysis of animal experiments.Frontiers in pharmacology · 2025Pooled it
- Effect of PCSK9 inhibitors on the quality of life in patients with acute coronary syndromes - exploratory analysis of the EMSIACS trial.Scientific reports · 2025Trial
- Integrated bioinformatics analysis reveals cross-talking hub genes and therapeutic agents between sepsis and acute myocardial infarction.Annals of medicine · 2026Article
- 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
- CCL17-neutralizing and esterase-responsive core-shell microgels for endogenous Tregs recruitment and functional enhancement in myocardial infarction.Bioactive materials · 2026Article
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Dendritic Cells in the Immunoregulation of Myocardial Infarction: Mechanisms and Therapeutic Strategies.Cardiovascular drugs and therapy · 2026Review
- Resibufogenin promotes angiogenesis via the VAV3-mediated ITGA5-VEGF signaling axis in macrophages to alleviate myocardial infarction.Acta pharmacologica Sinica · 2026Article
- Inflammasome inhibition in myocardial infarction reduces early reperfusion injury and suppresses systemic plaque activation.Atherosclerosis · 2026Article
- Chemistry and Biological Activity of 11Molecules (Basel, Switzerland) · 2026Review
- Parental Obesity and Offspring Risk for Cardiorenal Diseases.Current hypertension reports · 2026Review
- Programmable Paracrine-Mimetic Microneedle System for Temporal Regulation of Cardiac Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Toll-like receptor 7 constrains efferocytosis in myocardial injury.Basic research in cardiology · 2026Article
- miR-4443 alleviates myocardial injury in acute myocardial infarction by targeting and regulating TIMP2.Journal of thrombosis and thrombolysis · 2026Article
- SEM1 Downregulates HSPA8 to Suppress TLR4/MyD88/NF-κB Signaling and Alleviate Myocardial I/R Injury.International journal of molecular sciences · 2026Article
- Prediction of incident heart failure in men and women with a history of myocardial infarction.ESC heart failure · 2026Article
- Dynamic regulation of the 'mitochondria‑immune axis' in myocardial infarction: Molecular mechanisms driving macrophage polarization through energy metabolism disorders (Review).Molecular medicine reports · 2026Review
- Necroptosis is a key contributor to impaired cardiac repair following myocardial infarction.Cell death & disease · 2026Article
- Short-term blockade of E-prostanoid 3 receptor mitigates necroinflammation and ameliorates ischemia/reperfusion- and doxorubicin-induced acute myocardial injury.Basic research in cardiology · 2026Article
459 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
7 authors at 4 institutions in 5 countries.
Funding
Abstract
Acute myocardial infarction (AMI) and the heart failure that often follows, are major causes of death and disability worldwide. As such, new therapies are required to limit myocardial infarct (MI) size, prevent adverse left ventricular (LV) remodeling, and reduce the onset of heart failure following AMI. The inflammatory response to AMI, plays a critical role in determining MI size, and a persistent pro-inflammatory reaction can contribute to adverse post-MI LV remodeling, making inflammation an important therapeutic target for improving outcomes following AMI. In this article, we provide an overview of the multiple players (and their dynamic roles) involved in the complex inflammatory response to AMI and subsequent LV remodeling, and highlight future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size, preventing adverse LV remodeling, and reducing heart failure in AMI patients.
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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.