ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2023
CX3CR1 regulates the development of renal interstitial fibrosis through macrophage polarization.
Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- AMSC-EVs attenuate acute kidney injury through TXNIP-IKKα/NFκB signaling-mediated renal CX3CR1Stem cell research & therapy · 2025Article
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6 authors at 1 institution in 1 country.
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Abstract
objectivesThe binding of CX3C chemokine receptor 1 (CX3CR1) and its unique ligand CX3C chemokine ligand 1 (CX3CL1) can promote the migration of inflammatory cells to the lesion and affect the progression of renal interstitial fibrosis, but the underlying mechanisms remain unclear. This study aims to investigate whether CX3CR1 affects renal interstitial fibrosis by macrophage polarization.
methodsA mouse model of renal interstitial fibrosis was established by unilateral ureteral obstruction (UUO). C57/B6 mice were divided into a CX3CR1 inhibitor group (injected with CX3CR1 inhibitor AZD8797) and a model group (injected with physiological saline). After continuous intraperitoneal injection for 5 days, the ligated lateral kidneys of mice were obtained on the 7th day. Hematoxylin and eosin (HE) staining and Masson staining were used to observe the infiltration of inflammatory cells and the collagen fiber deposition in renal interstitium, respectively. The mRNA and protein expressions of CX3CR1, alpha-smooth muscle actin (
resultsThe infiltration of inflammatory cells and the collagen fiber deposition in renal interstitium were significantly reduced in the CX3CR1 inhibitor group. The mRNA and protein levels of
conclusionsInhibiting CX3CR1 can effectively prevent the progression of renal interstitial fibrosis. The mechanism may be related to macrophage polarization towards M2 type and upregulation of Arg-1 expression.
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