ReviewInternational journal of molecular sciences2020
Macrophage Phenotype and Fibrosis in Diabetic Nephropathy.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.
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Who cites it
145 citing papers in PubMed, 1 synthesis or guideline pooled it, 244 citations in OpenAlex.
- Focus on podocytes: diabetic kidney disease and renal fibrosis - a global bibliometric analysis (2000-2024).Frontiers in pharmacology · 2024Pooled it
- A bibliometric analysis of trace elements and diabetic kidney disease: scientific hotspots and research evolution.Renal failure · 2026Review
- Macrophage FOXO1 Inhibition Protects Against Hyperglycaemia-Associated Kidney Injury.Basic & clinical pharmacology & toxicology · 2026Article
- New insights into diagnostic values and mechanisms of ferroptosis associated with immune infiltration in diabetic kidney disease.Experimental and therapeutic medicine · 2026Article
- M1 macrophage-derived exosomes aggravate diabetic nephropathy by regulating the WTAP/S1PR2 axis.Journal of diabetes investigation · 2026Article
- Trained immunity: New insights into pathogenesis and therapeutic targets in diabetes and diabetic complications.Genes & diseases · 2026Review
- Aloin attenuates high-glucose-induced oxidative and inflammatory damage in renal cells via AMPK/Nrf2 signaling.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Human umbilical cord mesenchymal stromal cell-derived exosomes from MSCs pretreated with inflammatory factors attenuate renal injury of diabetic mice by regulating macrophage polarization.Clinical science (London, England : 1979) · 2026Article
- Mechanisms by which macrophage Ltb4r1 mediates tubular epithelial cell injury to facilitate the advancement of diabetic kidney disease.BMC nephrology · 2026Article
- Growth Differentiation Factor-15 in Diabetic Kidney and Cardiovascular Disease: Pathogenic Driver or Protective Modulator.Diabetes · 2026Review
- The role of immunoproteasome in diabetes and diabetes-related complications.Genes & diseases · 2026Review
- Linderalactone mitigates diabetic renal injury by inhibiting macrophage inflammation via the Dectin1/Syk/CARD9/IRF5/NF-κB pathway.Journal of diabetes investigation · 2026Article
- Mesenchymal Stem Cell-Derived Exosomes miR-143-3p Attenuates Diabetic Kidney Disease by Enhancing Podocyte Autophagy via Bcl-2/Beclin1 Pathway.Biomedicines · 2026Article
- Knowledge Mapping of Macrophages in Renal Fibrosis: A Bibliometric Analysis from 2014 to 2025.Journal of inflammation research · 2026Review
- Single-Cell Maps Reveal Novel Mechanisms of Ferroptosis and Biomarkers in Diabetic Nephropathy.Current medicinal chemistry · 2026Article
- Single-nucleus transcriptomics identifies SPON1 as a candidate mediator of the anti-fibrotic effect ofAmerican journal of translational research · 2026Article
- Heterogeneity characterization and key pathogenic genes screening based on diabetic nephropathy microenvironment.Open life sciences · 2026Article
- Unveiling the immune microenvironment in diabetic nephropathy: from mechanisms to therapeutics.Frontiers in immunology · 2026Review
- Maresin 1 Ameliorates Diabetic Kidney Disease in Mice by Promoting Macrophage M2 Polarization.Mediators of inflammation · 2026Article
- WTAP-induced mCell biochemistry and biophysics · 2025Article
85 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease globally. The primary initiating mechanism in DN is hyperglycemia-induced vascular dysfunction, but its progression is due to different pathological mechanisms, including oxidative stress, inflammatory cells infiltration, inflammation and fibrosis. Macrophages (Mφ) accumulation in kidneys correlates strongly with serum creatinine, interstitial myofibroblast accumulation and interstitial fibrosis scores. However, whether or not Mφ polarization is involved in the progression of DN has not been adequately defined. The prevalence of the different phenotypes during the course of DN, the existence of hybrid phenotypes and the plasticity of these cells depending of the environment have led to inconclusive results. In the same sense the role of the different macrophage phenotype in fibrosis associated or not to DN warrants additional investigation into Mφ polarization and its role in fibrosis. Due to the association between fibrosis and the progressive decline of renal function in DN, and the role of the different phenotypes of Mφ in fibrosis, in this review we examine the role of macrophage phenotype control in DN and highlight the potential factors contributing to phenotype change and injury or repair in DN.
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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.