ArticleTechnology and health care : official journal of the European Society for Engineering and Medicine2024
Cyclophosphamide ameliorates membranous nephropathy by upregulating miR-223 expression, promoting M2 macrophage polarization and inhibiting inflammation.
Article in Technology and health care : official journal of the European Society for Engineering and Medicine, 2024. 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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Who cites it
3 citing papers in PubMed.
- The role of interleukin-4 in acute kidney injury and chronic kidney disease: a literature review.BMC nephrology · 2026Review
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- Cyclophosphamide for severe T-DXd-induced interstitial lung disease in low-HER2 breast cancer: a case report and mechanistic insights.Frontiers in oncology · 2025Article
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Authors and funding
5 authors.
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Abstract
backgroundMembranous nephropathy (MN), also known as membranous glomerulonephritis, is a leading cause of adult nephrotic syndrome. The main pathological features encompass the deposition of immune complexes within the glomerular basement membrane epithelial cells, thickening of the basement membrane, and fusion of the foot process.
objectiveThis study aims to investigate the role of the immune and inflammatory modulator miR-223 in the immunosuppressive and anti-inflammatory effects of cyclophosphamide (CTX) on membranous nephropathy (MN).
methodsmiR-223 mimetics or inhibitors was used to regulate miR-223 levels. LPS induced inflammatory cell model and cell polarization. CTX was used to treat Lipopolysaccharides (LPS) induced inflammatory response and polarization. Cationic bovine serum albumin (c-BSA) induced BALB/c mouse MN model, while CTX was used to treat c-BSA induced MN.
resultsThe miR-223 level in LPS induced inflammatory model cells was lower than that in control cells. The levels of inflammatory factors in LPS+miR-223 mimetics and CTX+miR-223i cells were lower than those in LPS and miR-223i cells. The protein levels of LPS+miR-223 mimic, CTX+miR-223i macrophage M2 phenotype markers Arginase-1 (Arg1), transforming growth factor β1 (TGF-β1), anti-inflammatory factors interleukin-4 (IL4) and interleukin-13 (IL13) were significantly higher than those of LPS and miR-223i. The effect of CTX was confirmed in a BALB/c mouse MN model induced by cationic bovine serum albumin (c-BSA).
conclusionCTX upregulates the expression of miR-223, promotes polarization of M2 macrophages, alleviates the inflammatory response and renal injury of MN.
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