ArticleJournal of cellular and molecular medicine2019
Chemerin/ChemR23 axis promotes inflammation of glomerular endothelial cells in diabetic nephropathy.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Chemerin levels in chronic kidney disease: A systematic review and meta-analysis.Frontiers in endocrinology · 2023Pooled it
- Exploring the renoprotective potential of Beta vulgaris in diabetic nephropathy: an integrated network pharmacology, molecular docking and dynamics simulation study.Molecular diversity · 2026Article
- Adipokine networks in diabetic kidney disease: mechanistic insights and therapeutic implications.Lipids in health and disease · 2026Review
- ZBP1 Mediates Renal Tubular Injury in Diabetic Nephropathy Through RIPK3-mediated Necroptosis.Inflammation · 2026Article
- Translational advances in diabetic nephropathy management: integrating nanoformulation-based drug delivery systems.Frontiers in medical technology · 2026Review
- Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026Review
- Icariside II inhibits ferroptosis and improves high-glucose-induced podocytes injury by downregulating DNMT1.In vitro cellular & developmental biology. Animal · 2026Article
- Chemerin and Asprosin as Promising Biomarkers of Metabolic Syndrome: A Scoping Review.Current obesity reports · 2025Article
- Fetuin-A and Heme Oxygenase 1 as Potential New Markers in the Diagnosis of Diabetic Kidney Disease.International journal of molecular sciences · 2025Review
- Evaluating Feature Selection Methods for Accurate Diagnosis of Diabetic Kidney Disease.Biomedicines · 2024Article
- β-Arrestin-2 enhances endoplasmic reticulum stress-induced glomerular endothelial cell injury by activating transcription factor 6 in diabetic nephropathy.World journal of diabetes · 2024Article
- Proanthocyanidin offers protection against diabetic nephropathy: elucidation of its mechanism of action using animal models.Pharmaceutical biology · 2024Review
- The Role of Chemerin in Upper Gastrointestinal Cancer.Metabolites · 2024Review
- Bioinformatics to Identify Biomarkers of Diabetic Nephropathy based on Sphingolipid Metabolism and their Molecular Mechanisms.Current diabetes reviews · 2024Article
- Inflammatory Markers Used as Predictors of Subclinical Atherosclerosis in Patients with Diabetic Polyneuropathy.Life (Basel, Switzerland) · 2023Article
- The Importance of M1-and M2-Polarized Macrophages in Glioma and as Potential Treatment Targets.Brain sciences · 2023Review
- SGLT2 Inhibitors in the Treatment of Diabetic Kidney Disease: More than Just Glucose Regulation.Pharmaceutics · 2023Review
- The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023Review
- Recent Advances in the Emerging Therapeutic Strategies for Diabetic Kidney Diseases.International journal of molecular sciences · 2022Review
- Immunohistochemical expression of osteopontin and collagens in choroid plexus of human brains.Neuropathology : official journal of the Japanese Society of Neuropathology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is characterized by inflammation of renal tissue. Glomerular endothelial cells (GEnCs) play an important role in inflammation and protein leakage in urine in DN patients. Chemerin and its receptor ChemR23 are inducers of inflammation. The aim of this study was to investigate the function of chemerin/ChemR23 in GEnCs of DN patients. Immunohistochemical staining and qRT-PCR were used to measure the expression of chemerin, ChemR23 and inflammatory factors in renal tissues of DN patients. Db/db mice were used as animal model. ChemR23 of DN mice was knocked down by injecting LV3-shRNA into tail vein. Inflammation, physiological and pathological changes in each group was measured. GEnCs were cultured as an in vitro model to study potential signalling pathways. Results showed that expression of chemerin, ChemR23 and inflammatory factors increased in DN patients and mice. LV3-shRNA alleviated renal damage and inflammation in DN mice. GEnCs stimulated by glucose showed increased chemerin, ChemR23 and inflammatory factors and decreased endothelial marker CD31. Both LV3-shRNA and SB203580 (p38 MAPK inhibitor) attenuated chemerin-induced inflammation and injury in GEnCs. Taken together, chemerin/ChemR23 axis played an important role in endothelial injury and inflammation in DN via the p38 MAPK signalling pathway. Suppression of ChemR23 alleviated DN damage.
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