ReviewFrontiers in immunology2022
The role of the macrophage-to-myofibroblast transition in renal fibrosis.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 79 citations in OpenAlex.
- The inflammatory-autophagy-NETs axis in renal fibrosis: mechanistic crosstalk and pathological feed-forward amplification loops.Molecular and cellular biochemistry · 2026Review
- TREM2 in Macrophages Promotes Renal Fibrosis via Activation of β-Catenin Signalling Pathway in Obstructive Nephropathy.Cell proliferation · 2026Article
- S100A9 Aggravates Cardiac Fibrosis by TLR4/PGC-1α Mediated Macrophage-Myofibroblast Crosstalk.Journal of extracellular vesicles · 2026Article
- Curcumin Inhibits Renal Fibrosis by Suppressing S100A8/A9-TLR4 Signaling via Gut Microbiota-Derived Short-Chain Fatty Acid in Macrophages.Molecular nutrition & food research · 2026Article
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- The HDAC1 inhibitor attenuates renal ischemia-reperfusion injury via dual epigenetic modulation of p53 and macrophage NF-κB pathways.Cell biology and toxicology · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Applying dendrimer nanoprobes to the diagnosis and evaluation of kidney fibrosis.Nanomedicine (London, England) · 2026Review
- Developmental Programming of Kidney Disease Across the Life Course: A Narrative Review Focused on Inflammation.International journal of molecular sciences · 2026Review
- The role of immune cell crosstalk and signaling pathways in the pathogenesis of pulmonary fibrosis.Molecular biology reports · 2026Review
- RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206Frontiers in pharmacology · 2026Article
- Renal allograft interstitial fibrosis: multicellular interactions and therapeutic strategies.Frontiers in immunology · 2026Review
- Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transitionPeerJ · 2026Article
- Nanomedicine-Driven Precision Therapy for Renal Fibrosis: From Mechanistic Insights to Kidney-Targeted Interventions.International journal of nanomedicine · 2026Review
- Advances in the Targeted Drug Delivery System for Renal Fibrosis.International journal of nanomedicine · 2026Review
- Targeting Macrophage-to-Myofibroblast Transition Mitigates Progression from Inflammation to Fibrosis in Rosacea.International journal of biological sciences · 2026Article
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- Friend or foe? The role of SIRT6 on macrophage polarized to M2 subtype in acute kidney injury to chronic kidney disease.Renal failure · 2025Review
4 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis causes structural and functional impairment of the kidney, which is a dominant component of chronic kidney disease. Recently, a novel mechanism, macrophage-to-myofibroblast transition (MMT), has been identified as a crucial component in renal fibrosis as a response to chronic inflammation. It is a process by which bone marrow-derived macrophages differentiate into myofibroblasts during renal injury and promote renal fibrosis. Here, we summarized recent evidence and mechanisms of MMT in renal fibrosis. Understanding this phenomenon and its underlying signal pathway would be beneficial to find therapeutic targets for renal fibrosis in chronic kidney disease.
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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 OpenQuestion graph.