ArticleiScience2023
Galectin-3 as TREM2 upstream factor contributes to lung ischemia-reperfusion injury by regulating macrophage polarization.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- Upregulation of CREB1 by Mycobacterium Tuberculosis Transcriptionally Activates TREM2 to Promote Macrophage M2 Polarization.Cell biochemistry and function · 2026Article
- Evolution in lung IRI cell death research: a 20-year global bibliometric study (2005-2024).Annals of medicine and surgery (2012) · 2026Review
- Galectin-3 Mediates Heme-Induced Multi-Organ Dysfunction by Modulating the Splenic Immune Microenvironment.Diseases (Basel, Switzerland) · 2026Article
- Triggering Receptor Expressed on Myeloid Cells-2 Regulates Innate Lymphoid Cell Levels in Bleomycin-Induced Pulmonary Fibrosis.The Kaohsiung journal of medical sciences · 2026Article
- TREM2-driven peripheral macrophage regulation in inflammatory diseases: implications extending beyond neurological disorders.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Macrophage Signaling Pathways in Health and Disease: From Bench to Bedside Applications.MedComm · 2025Review
- TREM2 signaling pathway in sepsis-induced acute lung injury: physiology, pathology, and therapeutic applications.Frontiers in medicine · 2025Review
- The KLF4/Galectin-3 cascade is a key determinant of tubular cell death and acute kidney injury.International journal of biological sciences · 2025Article
- The double-edged role and therapeutic potential of TREM2 in atherosclerosis.Biomarker research · 2024Review
- Protective innate immunity againstInfection and immunity · 2024Article
- Review
- Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung ischemia-reperfusion injury (LIRI) is a complex "aseptic" inflammatory response, macrophage play a pivotal role in the pathogenesis of LIRI. Galectin-3 (Gal3), a lectin implicated inflammation, has received limited attention in LIRI. Studies have reported Gal3 as a ligand for triggering receptor expressed on myeloid cell 2 (TREM2) in macrophages in Alzheimer's disease. Hence, we established LIRI C57BL/6 mice model and hypoxia/glucose deprivation and reoxygenation (OGD/R) model to investigate the relationship among Gal3, TREM2, and macrophage polarization. Our result demonstrated inhibition of Gal3 significantly reduced M1-type macrophage polarization while markedly increased M2-type in LIRI. In addition, we observed colocalization of Gal3 and TREM2 in macrophages, inhibition of Gal3 could recover the downregulation of TREM2 induced by LIRI while promoting TREM2 expression could attenuate lung injury in LIRI. In summary, our findings suggest Gal3 as an upstream factor of TREM2, play a crucial role in LIRI by regulating macrophage polarization.
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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.