ArticleCell death & disease2021
Wnt5a promotes renal tubular inflammation in diabetic nephropathy by binding to CD146 through noncanonical Wnt signaling.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 54 citations in OpenAlex.
- Tiki2 restrains Wnt5a/Ror signaling to limit inflammation in acute kidney injury.Communications biology · 2026Article
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Biological properties of soluble CD146 and its role and mechanisms in disease progression.Frontiers in immunology · 2026Review
- The Association of Diabetes and Atherosclerosis: Understanding the Molecular Mechanism of the Double Burden.Current medicinal chemistry · 2026Review
- The multifaceted roles of MCAM in development, homeostasis, pathological conditions, and cancer.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Tubular Injury in Diabetic Kidney Disease: Early Diagnosis and Intervention Strategies.Diabetes/metabolism research and reviews · 2025Review
- Targeting WNT5A noncanonical signaling attenuates renal fibrosis progression in acute kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Prrx1 promotes mesangial cell proliferation and kidney fibrosis through YAP in diabetic nephropathy.Journal of pharmaceutical analysis · 2025Article
- Soluble CD146 in Heart Failure: Pathophysiological Role and Diagnostic Potential.Biomedicines · 2025Review
- Downregulation of S100 calcium-binding A4 (S100A4) ameliorates hepatic fibrosisEuropean journal of histochemistry : EJH · 2025Article
- Single-cell and spatial transcriptomic profiling revealed niche interactions sustaining growth of endometriotic lesions.Cell genomics · 2025Article
- Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease.Science advances · 2024Article
- Complement Cascade Proteins Correlate with Fibrosis and Inflammation in Early-Stage Type 1 Diabetic Kidney Disease in the Ins2Akita Mouse Model.International journal of molecular sciences · 2024Article
- Myricetin induces M2 macrophage polarization to alleviate renal tubulointerstitial fibrosis in diabetic nephropathyWorld journal of diabetes · 2024Article
- WNTA5-mediated miR-374a-5p regulates vascular smooth muscle cell phenotype transformation and M1 macrophage polarization impacting intracranial aneurysm progression.Scientific reports · 2024Article
- Comprehensive strategy for identifying extracellular vesicle surface proteins as biomarkers for chronic kidney disease.Frontiers in physiology · 2024Review
- Molecular mechanisms and therapeutic potential of natural flavonoids in diabetic nephropathy: Modulation of intracellular developmental signaling pathways.Current research in pharmacology and drug discovery · 2024Review
- Associations of Wnt5a expression with liver injury in chronic hepatitis B virus infection.BMC infectious diseases · 2023Article
- Transcriptional Comparison of Human and Murine Retinal Neovascularization.Investigative ophthalmology & visual science · 2023Article
- Endothelial Dysfunction in Cardiorenal Conditions: Implications of Endothelial Glucocorticoid Receptor-Wnt Signaling.International journal of molecular sciences · 2023Review
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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
Immune and inflammatory factors have emerged as key pathophysiological mechanisms in the progression of diabetic renal injury. Noncanonical Wnt5a signaling plays an essential role in obesity- or diabetes-induced metabolic dysfunction and inflammation, but its explicit molecular mechanisms and biological function in diabetic nephropathy (DN) remain unknown. In this study, we found that the expression of Wnt5a and CD146 in the kidney and the level of soluble form of CD146 (sCD146) in serum and urine samples were upregulated in DN patients compared to controls, and this alteration was correlated with the inflammatory process and progression of renal impairment. Blocking the activation of Wnt5a signaling with the Wnt5a antagonist Box5 prevented JNK phosphorylation and high glucose-induced inflammatory responses in db/db mice and high glucose-treated HK-2 cells. Similar effects were observed by silencing Wnt5a with small-interfering RNA (siRNA) in cultured HK-2 cells. Knockdown of CD146 blocked Wnt5a-induced expression of proinflammatory cytokines and activation of JNK, which suggests that CD146 is essential for the activation of the Wnt5a pathway. Finally, we confirmed that Wnt5a directly interacted with CD146 to activate noncanonical Wnt signaling in HK-2 cells. Taken together, our findings suggest that by directly binding to CD146, Wnt5a-induced noncanonical signaling is a contributing mechanism for renal tubular inflammation in diabetic nephropathy. The concentration of sCD146 in serum and urine could be a potential biomarker to predict renal outcomes in DN patients.
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