ArticleActa pharmacologica Sinica2018
Inflammation-activated CXCL16 pathway contributes to tubulointerstitial injury in mouse diabetic nephropathy.
Article in Acta pharmacologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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30 citing papers in PubMed, 44 citations in OpenAlex.
- Imbalance of mitochondria and abnormalities in lipid metabolism in Diabetic Tubulopathy.Annals of medicine · 2026Review
- Inhibiting the P2X7R-NLRP3 inflammasome pathway regulates CXCL16 to alleviate podocyte injury in mice with adriamycin nephropathy.Scientific reports · 2026Article
- Modeling kidney fibrosis and tubular regeneration in iPSC-derived kidney organoids.Stem cell research & therapy · 2025Article
- Gut microbiota: an important player in diabetic kidney disease.Diabetology & metabolic syndrome · 2025Review
- Identification and experimental validation of mitochondrial and endoplasmic reticulum stress related gene in diabetic nephropathy.Scientific reports · 2025Article
- Deficiency of Growth Arrest and DNA Damage-Inducible 45 α -R-Loop Pathway and Kidney Injury in Diabetic Nephropathy.Journal of the American Society of Nephrology : JASN · 2025Article
- An update on renal tubular injury as related to glycolipid metabolism in diabetic kidney disease.Frontiers in pharmacology · 2025Review
- Immune inflammation and metabolic interactions in the pathogenesis of diabetic nephropathy.Frontiers in endocrinology · 2025Review
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- Lipid nephrotoxicity mediated by HIF-1α activation accelerates tubular injury in diabetic nephropathy.Renal failure · 2024Article
- Renal transcriptome analysis of uninephrectomized db/db mice identified a mechanism for the transition to severe diabetic nephropathy.Experimental animals · 2024Article
- Inhibition of EZH2 mitigates peritoneal fibrosis and lipid precipitation in peritoneal mesothelial cells mediated by klotho.Renal failure · 2023Article
- [HIF-1α activation induces cholesterol homeostasis dysfunction to accelerate progression of diabetic nephropathy in rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Tanshinone IIA down-regulates -transforming growth factor beta 1 to relieve renal tubular epithelial cell inflammation and pyroptosis caused by high glucose.Bioengineered · 2022Article
- PAI-1 is a vascular cell-specific HIF-2-dependent angiogenic factor that promotes retinal neovascularization in diabetic patients.Science advances · 2022Article
- Baicalin attenuates adriamycin-induced nephrotic syndrome by regulating fibrosis procession and inflammatory reaction.Genes & genomics · 2021Article
- Metformin attenuates diabetic renal injury via the AMPK-autophagy axis.Experimental and therapeutic medicine · 2021Article
- RNA-Seq analysis reveals critical transcriptome changes caused by sodium butyrate in DN mouse models.Bioscience reports · 2021Article
- Article
- Using Machine Learning to Evaluate the Role of Microinflammation in Cardiovascular Events in Patients With Chronic Kidney Disease.Frontiers in immunology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation and lipid disorders play crucial roles in synergistically accelerating the progression of diabetic nephropathy (DN). In this study we investigated how inflammation and lipid disorders caused tubulointerstitial injury in DN in vivo and in vitro. Diabetic db/db mice were injected with 10% casein (0.5 mL, sc) every other day for 8 weeks to cause chronic inflammation. Compared with db/db mice, casein-injected db/db mice showed exacerbated tubulointerstitial injury, evidenced by increased secretion of extracellular matrix (ECM) and cholesterol accumulation in tubulointerstitium, which was accompanied by activation of the CXC chemokine ligand 16 (CXCL16) pathway. In the in vitro study, we treated HK-2 cells with IL-1β (5 ng/mL) and high glucose (30 mmol/L). IL-1β treatment increased cholesterol accumulation in HK-2 cells, leading to greatly increased ROS production, ECM protein expression levels, which was accompanied by the upregulated expression levels of proteins in the CXCL16 pathway. In contrast, after CXCL16 in HK-2 cells was knocked down by siRNA, the IL-1β-deteriorated changes were attenuated. In conclusion, inflammation accelerates renal tubulointerstitial lesions in mouse DN via increasing the activity of CXCL16 pathway.
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