ArticleKidney international2017
Targeted disruption of Cd40 in a genetically hypertensive rat model attenuates renal fibrosis and proteinuria, independent of blood pressure.
Article in Kidney international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
- Advances in Genome Editing and Application to the Generation of Genetically Modified Rat Models.Frontiers in genetics · 2021Review
- CD40/CD40L Signaling as a Promising Therapeutic Target for the Treatment of Renal Disease.Journal of clinical medicine · 2020Review
- CD40 Receptor Knockout Protects against Microcystin-LR (MC-LR) Prolongation and Exacerbation of Dextran Sulfate Sodium (DSS)-Induced Colitis.Biomedicines · 2020Article
- Renal Fibrosis Is Significantly Attenuated Following Targeted Disruption ofJournal of the American Heart Association · 2020Article
- Salt-sensitive increase in macrophages in the kidneys of Dahl SS rats.American journal of physiology. Renal physiology · 2019Article
- Cardiotonic Steroids and the Sodium Trade Balance: New Insights into Trade-Off Mechanisms Mediated by the Na⁺/K⁺-ATPase.International journal of molecular sciences · 2018Review
- Na/K-ATPase/src complex mediates regulation of CD40 in renal parenchyma.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2018Article
- Targeted disruption of regulated endocrine-specific protein ( Resp18) in Dahl SS/Mcw rats aggravates salt-induced hypertension and renal injury.Physiological genomics · 2018Article
- Inflammation and renal fibrosis: Recent developments on key signaling molecules as potential therapeutic targets.European journal of pharmacology · 2018Review
- Circulating CD40 and sCD40L Predict Changes in Renal Function in Subjects with Chronic Kidney Disease.Scientific reports · 2017Article
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Authors and funding
18 authors at 3 institutions in 1 country.
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Abstract
High blood pressure is a common cause of chronic kidney disease. Because CD40, a member of the tumor necrosis factor receptor family, has been linked to the progression of kidney disease in ischemic nephropathy, we studied the role of Cd40 in the development of hypertensive renal disease. The Cd40 gene was mutated in the Dahl S genetically hypertensive rat with renal disease by targeted-gene disruption using zinc-finger nuclease technology. These rats were then given low (0.3%) and high (2%) salt diets and compared. The resultant Cd40 mutants had significantly reduced levels of both urinary protein excretion (41.8 ± 3.1 mg/24 h vs. 103.7 ± 4.3 mg/24 h) and plasma creatinine (0.36 ± 0.05 mg/dl vs. 1.15 ± 0.19 mg/dl), with significantly higher creatinine clearance compared with the control S rats (3.04 ± 0.48 ml/min vs. 0.93 ± 0.15 ml/min), indicating renoprotection was conferred by mutation of the Cd40 locus. Furthermore, the Cd40 mutants had a significant attenuation in renal fibrosis, which persisted on the high salt diet. However, there was no difference in systolic blood pressure between the control and Cd40 mutant rats. Thus, these data serve as the first evidence for a direct link between Cd40 and hypertensive nephropathy. Hence, renal fibrosis is one of the underlying mechanisms by which Cd40 plays a crucial role in the development of hypertensive renal disease.
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