ArticleRenal failure2025
ALKBH5 induces macrophage activation to promote renal fibrosis via Retnla.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Functional Role of ALKBH5 in Kidney Injury: Insights Into Mechanisms and Therapeutic Potential.Journal of cellular biochemistry · 2026Review
- An Integrated Therapeutic Strategy for Cardiorenal Syndrome to Target Oxidative Stress, Inflammation, and Fibrosis.Reviews in cardiovascular medicine · 2026Review
- RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206Frontiers in pharmacology · 2026Article
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Authors and funding
9 authors.
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Abstract
Renal fibrosis is a common pathological endpoint of various chronic kidney diseases. Macrophages play an important role in the pathophysiological process of renal fibrosis. However, the exact function and molecular mechanism of macrophages during renal fibrosis remain unclear. In this study, we found an increased expression of RNA demethylase AlkB Homolog 5 (ALKBH5) in macrophages from the mice with unilateral ureteral obstruction (UUO) and TGF-β treatments bone marrow-derived macrophages. Macrophage-specific ALKBH5 knockout could significantly alleviate renal fibrosis in UUO mice and decrease the infiltration of macrophages in the kidneys. Further studies showed that ALKBH5 deficiency reduced M2a macrophage polarization and the expression of TGF-β1, Arg1, and CD206 both
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