ReviewJournal of advanced research2026
Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.
Review 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 10 papers.
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
10 citing papers in PubMed.
- Allosteric activation of Trx1 by antagonizing nitrative modification at tyrosine 49 confers neuroprotection against ischemic stroke.Redox biology · 2026Article
- The NETs-cGAS-STING Axis in Ischemic Stroke: Linking Neutrophil-Microglia Crosstalk, Immunothrombosis, and Neuroinflammation.Molecular neurobiology · 2026Review
- Protective Effects of Ranolazine in a Rat Model of Ovarian Ischemia/Reperfusion Injury.International journal of molecular sciences · 2026Article
- Qishen Granules attenuate adverse ventricular remodeling in chronic heart failure by promoting Legumain/Arg1/Rac1-mediated efferocytosis of resident cardiac macrophages.Chinese medicine · 2026Article
- Leonurine alleviates lung ischemia-reperfusion injury through suppression of ferroptosis via RORα in male mice.The Journal of endocrinology · 2026Article
- Ginsenoside Rg1 Attenuates Renal Ischemia-Reperfusion Injury and Fibrosis by Suppressing Pro-Inflammatory Macrophage Activation.Journal of inflammation research · 2026Article
- PANoptosis nexus in ischemia-reperfusion injury: from integrated cell death mechanisms to novel therapeutic opportunities.Frontiers in immunology · 2026Review
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- Mechanistic elucidation of Wuling Powder targeting macrophage polarization to ameliorate renal ischemia-reperfusion injury via multidimensional computational systems pharmacology coupled with experimental validation.Frontiers in pharmacology · 2026Article
- Machine learning-based predictive model for the perioperative co-occurrence of T-cell-mediated rejection and pneumonia in liver transplantation.Frontiers in immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemia-Reperfusion Injury (IRI) is a complex pathophysiological process characterized by oxidative stress and inflammatory responses during tissue reperfusion, leading to severe organ dysfunction. Macrophages, as key immune cells, play a pivotal role in the pathogenesis of IRI, exhibiting dynamic functions that influence both tissue damage and repair. Despite extensive research, the precise mechanisms underlying macrophage-mediated IRI remain incompletely understood, necessitating a comprehensive review to explore their multifaceted roles and potential therapeutic targets. AIM OF REVIEW: This review aims to elucidate the diverse roles of macrophages in IRI, focusing on their involvement in programmed cell death mechanisms, communication with other immune cells, and regulatory effects on key organs affected by IRI. The review also explores potential therapeutic strategies targeting macrophages to mitigate IRI-induced injury. Key Scientific Concepts of Review: This article reviews the multifaceted roles of macrophages in IRI and explores various modes of macrophage programmed cell death induced by IRI, including gasdermin D-mediated pyroptosis, lipid peroxidation-associated ferroptosis, PARP-1-mediated PAR-dependent cell death, PANoptosis regulated by the PANoptosome, and the formation of macrophage extracellular traps (METs) induced by both reactive oxygen species-dependent and -independent pathways. Additionally, it discusses intercellular communication between macrophages and other immune cells in IRI, focusing on the bidirectional regulatory effects between macrophages and neutrophils, as well as their synergistic role in resolving inflammation. Moreover, the regulatory mechanisms of macrophages in IRI affecting key organs, such as the brain, lung, heart, kidneys and liver, have been systematically summarized. Finally, innovative therapeutic strategies targeting macrophages, including precise approaches such as regulating cell polarization, inhibiting excessive METs formation, and utilizing nano-drug delivery systems, are thoroughly analyzed. This review provides a significant theoretical foundation for clinical translational research on IRI.
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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 Socratic graph.