ReviewFrontiers in physiology2020
Metabolic Modulation of Macrophage Function Post Myocardial Infarction.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Lipoprotein(a) and oxidized phospholipids are associated with myocardial inflammation after acute myocardial infarction.Nature cardiovascular research · 2026Trial
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Serotonin 5-HT7 receptor signaling modulates inflammatory responses and survival after myocardial infarction.Journal of translational medicine · 2026Article
- A call to redefine cardiovascular immunobiology around leukocyte plasticity.American journal of physiology. Heart and circulatory physiology · 2026Article
- Pharmacological upregulation of macrophage-derived itaconic acid by pubescenoside C attenuated myocardial ischemia-reperfusion injury.Journal of advanced research · 2025Article
- Macrophage polarization in acute myocardial infarction: multidimensional regulation and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges.Nature reviews. Cardiology · 2023Review
- Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction.Cellular & molecular biology letters · 2023Review
- The cardiac wound healing response to myocardial infarction.WIREs mechanisms of disease · 2023Review
- Mitochondrial metabolism in macrophages.American journal of physiology. Cell physiology · 2021Review
- Mechanisms and strategies for a therapeutic cardiac immune response.Journal of molecular and cellular cardiology · 2021Article
- Sodium Lactate Accelerates M2 Macrophage Polarization and Improves Cardiac Function after Myocardial Infarction in Mice.Cardiovascular therapeutics · 2021Article
- Considering Cause and Effect of Immune Cell Aging on Cardiac Repair after Myocardial Infarction.Cells · 2020Review
- Regenerative and molecular therapies for myocardial repair (Review).Medicine internationalReview
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
Abstract
Macrophages are key components of innate immunity, and they play critical roles in heart health and diseases. Following acute myocardial infarction (MI), infiltrating macrophages undergo drastic phenotypic transition from pro-inflammatory in the early stage to pro-healing in the late stage. Transcriptome analyses of macrophage in the infarct zone show a time-dependent reprogramming of mitochondrial and metabolic functions, which parallels the changes of macrophage function. These observations suggest that mitochondrial and metabolic targets could be exploited for therapeutic opportunities. In this article, we reviewed the recent work on immunometabolic features of macrophage over the MI time continuum. In addition, we summarized currently proposed mitochondrial pathways involved in the functional polarization of macrophage and discussed their potential relevance to the outcome of MI. We expect that these findings will stimulate further investigations in metabolic modulation of innate immunity in the post-MI setting, which could ultimately lead to new strategies for therapy.
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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.