ArticleJournal of the American Society of Nephrology : JASN2013
Genetic deletion of cell division autoantigen 1 retards diabetes-associated renal injury.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Complement 5a receptor 2 attenuates diabetic kidney disease by promoting mitochondria-associated endoplasmic reticulum membrane formation mediated by PSS-MFN2 interaction.Cell discovery · 2026Article
- Induced Genetic Deletion of Cell Division Autoantigen 1 in Adulthood Attenuates Diabetes-Associated Renal Fibrosis.International journal of molecular sciences · 2025Article
- To target cellular senescence in diabetic kidney disease: the known and the unknown.Clinical science (London, England : 1979) · 2024Review
- TSPYL1 as a Critical Regulator of TGFβ Signaling through Repression of TGFBR1 and TSPYL2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- AAV9-Tspyl2 gene therapy retards bleomycin-induced pulmonary fibrosis by modulating downstream TGF-β signaling in mice.Cell death & disease · 2023Article
- Protection of diabetes in aortic abdominal aneurysm: Are antidiabetics the real effectors?Frontiers in cardiovascular medicine · 2023Review
- The Role of Cell Division Autoantigen 1 (CDA1) in Renal Fibrosis of Diabetic Nephropathy.BioMed research international · 2021Review
- TSPYL2 Regulates the Expression of EZH2 Target Genes in Neurons.Molecular neurobiology · 2019Article
- MiR-30e-5p and MiR-15a-5p Expressions in Plasma and Urine of Type 1 Diabetic Patients With Diabetic Kidney Disease.Frontiers in genetics · 2019Article
- The Y-located proto-oncogene TSPY exacerbates and its X-homologue TSPX inhibits transactivation functions of androgen receptor and its constitutively active variants.Human molecular genetics · 2017Article
- Podocyte-specific Nox4 deletion affords renoprotection in a mouse model of diabetic nephropathy.Diabetologia · 2016Article
- Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy.Journal of the American Society of Nephrology : JASN · 2014Article
- Novel targets of antifibrotic and anti-inflammatory treatment in CKD.Nature reviews. Nephrology · 2014Review
- Battle of the sexes: contrasting roles of testis-specific protein Y-encoded (TSPY) and TSPX in human oncogenesis.Asian journal of andrologyReview
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell division autoantigen 1 (CDA1) enhances TGF-β signaling in renal and vascular cells, and renal expression of CDA1 is elevated in animal models of diabetes. In this study, we investigated the genetic deletion of Tspyl2, the gene encoding CDA1, in C57BL6 and ApoE knockout mice. The increased renal expression of TGF-β1, TGF-β type I and II receptors, and phosphorylated Smad3 associated with diabetes in wild-type mice was attenuated in diabetic CDA1 knockout mice. Notably, CDA1 deletion significantly reduced diabetes-associated renal matrix accumulation and immunohistochemical staining for collagens III and IV and attenuated glomerular and tubulointerstitial injury indices, despite the presence of persistent hyperglycemia, polyuria, renal hypertrophy, and hyperfiltration. Furthermore, CDA1 deletion reduced gene expression of TGF-β1 receptors in the kidney, resulting in a functionally attenuated response to exogenous TGF-β, including reduced levels of phosphorylated Smad3 and ERK1/2, in primary kidney cells from CDA1 knockout animals. Taken together, these data suggest that CDA1 deletion reduces but does not block renal TGF-β signaling. Because direct antagonism of TGF-β or its receptors has unwanted effects, CDA1 may be a potential therapeutic target for retarding DN and perhaps, other kidney diseases associated with TGF-β-mediated fibrogenesis.
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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.