ArticleAging2021
The role of CDX2 in renal tubular lesions during diabetic kidney disease.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- LOX-induced tubulointerstitial fibrosis via the TGF-β/LOX/Snail axis in diabetic mice.Journal of translational medicine · 2025Article
- Alpha lipoamide inhibits diabetic kidney fibrosis via improving mitochondrial function and regulating RXRα expression and activation.Acta pharmacologica Sinica · 2023Article
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
- Cellular phenotypic transitions in diabetic nephropathy: An update.Frontiers in pharmacology · 2022Review
- Metformin Ameliorates Epithelial-Mesenchymal Transition of Renal Tubular Epithelial Cells in Diabetes by Increasing Vitamin D Receptor Expression.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Molecular and clinicopathological differences between depressed and protruded T2 colorectal cancer.PloS one · 2022Article
- Recent Advances in Diabetic Kidney Diseases: From Kidney Injury to Kidney Fibrosis.International journal of molecular sciences · 2021Review
- Administration of Nrf-2-Modified Hair-Follicle MSCs Ameliorates DSS-Induced Ulcerative Colitis in Rats.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubules are vulnerable targets of various factors causing kidney injury in diabetic kidney disease (DKD), and the degree of tubular lesions is closely related to renal function. Abnormal renal tubular epithelial cells (RTECs) differentiation and depletion of cell junction proteins are important in DKD pathogenesis. Caudal-type homeobox transcription factor 2 (CDX2), represents a key nuclear transcription factor that maintains normal proliferation and differentiation of the intestinal epithelium. The present study aimed to evaluate the effects of CDX2 on RTECs differentiation and cell junction proteins in DKD. The results demonstrated that CDX2 was mainly localized in renal tubules, and downregulated in various DKD models. CDX2 upregulated E-cadherin and suppressed partial epithelial-mesenchymal transition (EMT), which can alleviate hyperglycemia-associated RTECs injury. Cystic fibrosis transmembrane conductance regulator (CFTR) was regulated by CDX2 in NRK-52E cells, and CFTR interfered with β-catenin activation by binding to Dvl2, which is an essential component of Wnt/β-catenin signaling. CFTR knockdown abolished the suppressive effects of CDX2 on Wnt/β-catenin signaling, thereby upregulating cell junction proteins and inhibiting partial EMT in RTECs. In summary, CDX2 can improve renal tubular lesions during DKD by increasing CFTR amounts to suppress the Wnt/β-catenin signaling pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.