ArticleThe Journal of clinical investigation2023
Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
176 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.
- SIRT3 in post-myocardial infarction macrophage reprogramming: linking mitochondrial fitness to inflammation resolution and repair.Frontiers in immunology · 2026Pooled it
- Trial
- Mitochondria-derived peptide hydrogel augments mitochondrial transplantation for promoting cardiac repair via macrophage metabolic reprogramming.Bioactive materials · 2027Article
- SIK2 antagonizes postinfarction cardiac repair by driving macrophage proinflammatory and impairing efferocytosis.Science advances · 2026Article
- Modulatory effects of S1QEL on OxLDL-induced metabolic alterations and inflammatory responses in human monocytes.Immunometabolism (Cobham, Surrey) · 2026Article
- Targeting efferocytosis with carbonized polymer dots from a natural anti-inflammatory drug to alleviate excessive inflammatory responses in the acute phase of myocardial infarction.Materials today. Bio · 2026Article
- Macrophage peroxisomes at the crossroads of inflammation.Immunometabolism (Cobham, Surrey) · 2026Review
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Mitochondria-transplanted macrophages: a novel strategy targeting mitochondrial dysfunction to enhance myocardial repair after myocardial infarction.MedScience · 2026Article
- Vaginal Microbiota and Pelvic Floor Dysfunction: Mechanistic Insights and Therapeutic Implications.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- SR-A3 Promotes USP18-Mediated deISGylation of STING to Protect Against Myocardial Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell immune atlas of mouse testes unveils metabolic reprogramming of FOLR2 + macrophages in orchestrating testicular immunity during aging.GeroScience · 2026Article
- Mitochondrial Metabolic Biomarkers in Periodontitis: Discovery and Clinical Validation.International dental journal · 2026Article
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Aerobic exercise modulates macrophage polarization and promotes cardiac recovery after myocardial infarction in rats.Journal of cardiothoracic surgery · 2026Article
- The deubiquitinase USP4 stabilizes the SCFNature communications · 2026Article
- Role of Plant-Derived Antioxidants in Oxidative Stress-Associated Myocardial Infarction: Structure-Activity Relationship (SAR)-Based Mechanistic Insights.Molecules (Basel, Switzerland) · 2026Review
- MiR-378a-3p Promotes Macrophage Polarization from M1 to M2 for Cardiac Repair after Infarction Via Trem1.Journal of cardiovascular translational research · 2026Article
- Regulation of acute myocardial infarction by CircTMCC1 through mitochondrial dysfunction and AMPK/mTOR-driven M1 macrophage polarization: role in QFR assessment.Cell death discovery · 2026Article
- Protein lactylation in health and diseases: molecular mechanisms, biological significance, and clinical implications.Signal transduction and targeted therapy · 2026Review
116 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Innate immune cells play important roles in tissue injury and repair following acute myocardial infarction (MI). Although reprogramming of macrophage metabolism has been observed during inflammation and resolution phases, the mechanistic link to macrophage phenotype is not fully understood. In this study, we found that myeloid-specific deletion (mKO) of mitochondrial complex I protein, encoded by Ndufs4, reproduced the proinflammatory metabolic profile in macrophages and exaggerated the response to LPS. Moreover, mKO mice showed increased mortality, poor scar formation, and worsened cardiac function 30 days after MI. We observed a greater inflammatory response in mKO mice on day 1 followed by increased cell death of infiltrating macrophages and blunted transition to the reparative phase during post-MI days 3-7. Efferocytosis was impaired in mKO macrophages, leading to lower expression of antiinflammatory cytokines and tissue repair factors, which suppressed the proliferation and activation of myofibroblasts in the infarcted area. Mitochondria-targeted ROS scavenging rescued these impairments, improved myofibroblast function in vivo, and reduced post-MI mortality in mKO mice. Together these results reveal a critical role of mitochondria in inflammation resolution and tissue repair via modulation of efferocytosis and crosstalk with fibroblasts. These findings have potential significance for post-MI recovery as well as for other inflammatory conditions.
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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.