ArticleBMC nephrology2025
CD148 agonistic antibody alleviates renal injury induced by chronic angiotensin II infusion in mice.
Article in BMC nephrology, 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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Who cites it
3 citing papers in PubMed.
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Hypertension-Induced Renal Injury: From Pathophysiology to Therapeutic Perspectives.Biomedicines · 2026Review
- NAT10 induces N4-acetylcytidine modification of AdipoR1-mediated mitochondrial biogenesis against endothelial-to-mesenchymal transition in hypertension.Molecular medicine (Cambridge, Mass.) · 2025Article
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10 authors.
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Abstract
backgroundAngiotensin II (Ang II) plays a critical role in the progression of kidney disease. In addition to its direct signaling events, Ang II transactivates epidermal growth factor receptor (EGFR) and causes renal injury. CD148 is a transmembrane protein tyrosine phosphatase that dephosphorylates EGFR and strongly inhibits its activity. In this study, we have asked if CD148 agonistic antibody 18E1 mAb attenuates renal injury induced by chronic Ang II infusion to explore its therapeutic application.
methodsHypertensive nephropathy was induced in mice subjected to unilateral nephrectomy (UNx) by infusing Ang II (1.4 mg/kg per day) for 6 weeks using an osmotic minipump. The 18E1 mAb or isotype control IgG were intraperitoneally injected (15 mg/kg, three times per week) to the UNx + Ang II mice for 6 weeks, and their renal phenotype was investigated.
resultsChronic Ang II infusion induced evident hypertension and renal injury that is indicated by elevation of plasma creatinine, urinary albumin excretion, renal hypertrophy, podocyte injury, macrophage infiltration, and the expression of alpha smooth muscle actin and collagen deposition. As compared with isotype control antibody, 18E1 mAb significantly reduced these renal changes, while it showed no effects on blood pressure. Furthermore, phospho-EGFR immunohistochemistry and immunoblotting demonstrated renal EGFR is activated in the mice that were subjected to UNx and Ang II infusion and 18E1 mAb significantly reduces EGFR phosphorylation in these kidneys as compared with isotype control treatment.
conclusionAgonistic CD148 antibody attenuates UNx + Ang II-induced renal injury, in part by reducing EGFR activity.
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