ReviewFrontiers in physiology2021
The Role of Macrophages in Kidney Fibrosis.
Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 116 citations in OpenAlex.
- CCL5 mRNA-enriched small extracellular vesicles from renal tubular epithelial cells enhance macrophage inflammatory responses in diabetic nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Chimeric antigen receptor-macrophages: A new paradigm for cell therapy.Bioengineering & translational medicine · 2026Review
- Antifibrotic Effects of Yi-Qi-Jian-Pi-Xiao-Yu Formula in Kidney via HIF1A-Driven M1 Macrophage Polarization.Phytochemical analysis : PCA · 2026Article
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Empagliflozin and renal histological changes in an experimental model of heart failure in male rats.Physiological reports · 2026Article
- An Integrated Machine-Learning and Reverse Network-Pharmacology Pipeline RevealsInternational journal of molecular sciences · 2026Article
- Review
- GPR183 contributes to renal macrophage infiltration and fibrosis in kidney injury.American journal of physiology. Renal physiology · 2026Article
- Inflammation: The Pathological Axis of Cisplatin-Induced Renal Injury.Journal of inflammation research · 2026Review
- Indoleamine 2,3-dioxygenase-regulated macrophages metabolic reprogramming rescues tacrolimus-induced nephrotoxicity.Frontiers in pharmacology · 2026Article
- RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206Frontiers in pharmacology · 2026Article
- Integrative omics and experimental validation reveal METTL17 and SLC27A1 as biomarkers and potential therapeutic targets in chronic kidney disease.Frontiers in immunology · 2026Article
- Macrophages and TGFB signaling regulate fibrosis in theAmerican journal of physiology. Renal physiology · 2026Article
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- Metabolic glycoengineered exosome-A2M nanoplatform reprograms macrophage polarization and orchestrates bone regeneration in ONFH.Cell death discovery · 2025Article
- Taming renal inflammation: signaling pathways and therapeutic advances in lupus nephritis.BMC nephrology · 2025Review
- Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging.Nature communications · 2025Article
- Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Kidney Fibrosis In Vitro and In Vivo Models: Path Toward Physiologically Relevant Humanized Models.Advanced healthcare materials · 2025Review
- Progression of Kidney Fibrosis after Sepsis: Underestimated Role of Resident Macrophages and Recruited Monocytes.Journal of the American Society of Nephrology : JASN · 2025Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phenotypic heterogeneity and functional diversity of macrophages confer on them complexed roles in the development and progression of kidney diseases. After kidney injury, bone marrow-derived monocytes are rapidly recruited to the glomerulus and tubulointerstitium. They are activated and differentiated on site into pro-inflammatory M1 macrophages, which initiate Th1-type adaptive immune responses and damage normal tissues. In contrast, anti-inflammatory M2 macrophages induce Th2-type immune responses, secrete large amounts of TGF-β and anti-inflammatory cytokines, transform into αSMA+ myofibroblasts in injured kidney, inhibit immune responses, and promote wound healing and tissue fibrosis. Previous studies on the role of macrophages in kidney fibrosis were mainly focused on inflammation-associated injury and injury repair. Apart from macrophage-secreted profibrotic cytokines, such as TGF-β, evidence for a direct contribution of macrophages to kidney fibrosis is lacking. However, under inflammatory conditions, Wnt ligands are derived mainly from macrophages and Wnt signaling is central in the network of multiple profibrotic pathways. Largely underinvestigated are the direct contribution of macrophages to profibrotic signaling pathways, macrophage phenotypic heterogeneity and functional diversity in relation to kidney fibrosis, and on their cross-talk with other cells in profibrotic signaling networks that cause fibrosis. Here we aim to provide an overview on the roles of macrophage phenotypic and functional diversity in their contribution to pro-fibrotic signaling pathways, and on the therapeutic potential of targeting macrophages for the treatment of kidney fibrosis.
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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.