ArticleJournal of the American Heart Association2018
Inflammation, Autophagy, and Apoptosis After Myocardial Infarction.
Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 1 of them a synthesis that pooled it.
What it found
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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
148 citing papers in PubMed, 1 synthesis or guideline pooled it, 235 citations in OpenAlex.
- Research Progress of Electrical Stimulation in Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2021Pooled it
- Crocetin Attenuates Fibroblast-to-Myofibroblast Transition after Myocardial Infarction in Mice by Regulating Autophagy.Cardiovascular drugs and therapy · 2026Article
- Micropeptide SCAPEP triggers lung adenocarcinoma tumorigenesis via regulating autophagy by promoting CDK15-mediated phosphorylation of vimentin.Cell death & disease · 2026Article
- Article
- Heart Scar-In-A-Dish: Tissue Culture Platform to Study Myocardial Injury and Mechanics In Vitro.Journal of biomechanical engineering · 2026Article
- GATA4-overexpressing BMSCs-derived exosome regulation of myocardial infarction in mice by key miRNA and apoptosis gene CLU.European journal of medical research · 2026Article
- Evolocumab early reduces IL-1β/IL-17A and improves left ventricular function in STEMI: an observational study in the real world.Frontiers in pharmacology · 2026Article
- Qing-Xin-Jie-Yu Granule attenuates myocardial infarction-induced inflammatory response by regulating the MK2/TTP pathway.Pharmaceutical biology · 2025Article
- Targeted Anti-Inflammatory Therapy in Cardiovascular Events: Challenges and Opportunities.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- ER-phagy Activation by AMFR Attenuates Cardiac Fibrosis Post-Myocardial Infarction via mTORC1 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiac Macrophages Promote Polarization of Macrophages toward M2 Phenotype to Improve Myocardial Remodeling via NGAL after Myocardial Infarction.Cell biochemistry and biophysics · 2025Article
- S100A4-shRNA mitigates autophagy, reduces inflammation, and improves cardiac functionality in MIRI.International journal of cardiology. Cardiovascular risk and prevention · 2025Article
- Endothelial PRMT7 prevents dysfunction, promotes revascularization and enhances cardiac recovery post-myocardial infarction.Experimental & molecular medicine · 2025Article
- Xinnaotongluo liquid protects H9c2 cells against hypoxic damage through IRF2/HIF-1α-mediated oxidation, inflammation, and apoptosis.Histology and histopathology · 2025Article
- The contribution of cardiomyocyte hypercontracture to the burden of acute myocardial infarction: an update.Basic research in cardiology · 2025Review
- Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation.Cell communication and signaling : CCS · 2025Article
- Impact of sodium-glucose transport protein-2 (SGLT2) inhibitors on the inflammasome pathway in acute myocardial infarction in type 2 diabetes mellitus: a comprehensive review.Cardiovascular diabetology · 2025Review
- Integrating the Interleukins in the Biomarker Panel for the Diagnosis and Prognosis of Patients with Acute Coronary Syndromes: Unraveling a Multifaceted Conundrum.Diagnostics (Basel, Switzerland) · 2025Article
- Article
- Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025Review
88 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is evidence for inflammation, autophagy, and apoptosis in the ischemic heart. Autophagy is a physiologic process for tissue survival. Apoptosis, on the other hand, is a mechanism that serves to clear the debris in the setting of tissue injury. The balance between autophagy and apoptosis may be important in cell survival and cardiac function. METHODS AND
resultsWe examined the interplay of inflammation and myocyte autophagy and apoptosis during the ischemic process. We subjected mice to total left coronary artery ligation and studied these animals for up to 4 weeks. The inflammatory (tumor necrosis factor [TNF]-α, monocyte chemoattractant protein-1, interleukin-6, and interleukin-1β) and autophagic signals (light chain-3 and beclin-1) were strongest during the first week and then began to decline. However, the apoptotic signals peaked at week 2 after left coronary artery ligation, and the elevated levels persisted until the end of the fourth week. To elucidate the role of inflammation in the regulation of myocyte autophagy and apoptosis, we administered TNF-α inhibitor (CAS1049741-03-8, Millipore, Burlington, MA) to the mice daily during the first week of myocardial infarction. Anti-TNF-α therapy reduced the levels of inflammatory cytokines and the inflammatory cell infiltration in and around the infarct area. However, cardiac function measured by echocardiography (fractional shortening and ejection fraction) worsened with anti-TNF-α therapy. More importantly, application of TNF-α inhibitor markedly inhibited autophagy and promoted myocyte apoptosis in the border zone.
conclusionsThese observations suggest that inflammatory response may be protective in the early stage of the myocardial infarction through stimulation of myocyte autophagy. Anti-inflammatory treatment early after coronary occlusion may have an adverse effect.
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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.