ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
RasGRP4 Exacerbates Diabetic Kidney Fibrosis via Aloxe3-Mediated Oxidative Stress and Scar-Associated Macrophage Activation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Review
- RasGRP4 Exacerbates Diabetic Kidney Fibrosis via Aloxe3-Mediated Oxidative Stress and Scar-Associated Macrophage Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
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11 authors.
Funding
Abstract
Renal fibrosis is an irreversible pathological feature of diabetic kidney disease (DKD), and targeting macrophage phenotype is a promising strategy to prolong it. Ras guanine nucleotide-releasing protein 4 (RasGRP4) is a signaling protein involved in immune regulation. This study aimed to investigate how RasGRP4 contributes to kidney fibrosis by regulating scar-associated macrophages (SAM). Kidney biopsy tissues and peripheral blood mononuclear cells (PBMCs) were collected from diabetic patients. Findings indicated that RasGRP4-expressing macrophages infiltrated the kidneys more extensively, and RasGRP4 levels in PBMCs rose with the progression of proteinuria. The DKD model was constructed using RasGRP4 knockout mice to assess the impact of RasGRP4 on renal interstitial fibrosis. Transcriptomic sequencing of PBMCs revealed that RasGRP4
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