ArticleJournal of advanced research2026
Novel function of macrophage migration inhibitory factor in regulating post-infarct inflammation and the therapeutic significance.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A multicentre analysis of efficacy, safety and molecular response correlates of fostamatinib in warm autoimmune haemolytic anaemia and Evans syndrome.British journal of haematology · 2026Article
- Epithelial redox stress programs macrophage immunometabolism through a ZNF24-MIF-NF-κB pathway in chronic nonbacterial prostatitis.Redox biology · 2026Article
- Targeting Macrophage-Mediated Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Strategies.Journal of inflammation research · 2026Review
- Machine Learning, scRNA-Seq and Biological Experiments Identify Hub Genes Responsible for Ischemia-Reperfusion Injury in Steatotic Liver Allografts.Journal of inflammation research · 2026Article
- Ion channels and atrial fibrillation: mitophagy as a key mediator.Frontiers in physiology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionRecent studies indicate that macrophage migration inhibitory factor (MIF) has a dual role in myocardial infarction (MI), with different cellular sources of MIF influencing inflammation and healing differentially.
objectivesTo investigate the role and underlying mechanism of MIF in MI and interventional efficacy targeting MIF.
methodsWild-type (WT), global MIF gene knockout (KO) and chimeric mice were subjected to coronary artery occlusion. The inflammatory responses and healing processes following MI were studied in both in vivo and in vitro settings. Furthermore, the therapeutic potential of pharmacological MIF inhibition to improve the prognosis of MI was explored.
resultsGlobally, MIF enhanced systemic and local inflammatory responses, as well as splenic monocyte mobilization, in mice with MI. MIF promoted monocyte migration through CCR2 and CXCR4 in peripheral blood mononuclear cells (PBMCs) and the infarcted myocardium. Additionally, MIF augmented angiotensin Ⅱ type 1 receptor (AT-1R) expression and interacted with AT-1R to promote the splenic monocyte mobilization following acute MI. MIF derived from bone marrow cells (KO
conclusionDeletion of global and inflammatory-cell-derived MIF diminished inflammation following MI by inhibiting monocyte mobilization and downregulating pro-inflammatory mediators, while cardiac-derived MIF exerted anti-inflammatory influence and facilitated healing. Furthermore, MIF antibody therapy protected the heart from severe ischemic injury and improved long-term prognosis.
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