ArticleFrontiers in cell and developmental biology2022
TFP5-Mediated CDK5 Activity Inhibition Improves Diabetic Nephropathy
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- Unveiling the TrkA-p35/CDK5 axis: a novel therapeutic target in diabetic kidney disease.Frontiers in endocrinology · 2026Article
- Article
- Cdk5 mediates impaired autophagy by regulating NGF/Sirt1 axis to cause diabetic islet β cell damage.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
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Abstract
Diabetic nephropathy (DN) is one of the leading causes of chronic kidney disease (CKD), during which hyperglycemia is composed of the major force for the deterioration to end-stage renal disease (ESRD). However, the underlying mechanism triggering the effect of hyperglycemia on DN is not very clear and the clinically available drug for hyperglycemia-induced DN is in need of urgent development. Here, we found that high glucose (HG) increased the activity of cyclin-dependent kinase 5 (CDK5) dependent on P35/25 and which upregulated the oxidative stress and apoptosis of mouse podocytes (MPC-5). TFP5, a 25-amino acid peptide inhibiting CDK5 activity, decreased the secretion of inflammation cytokines in serum and kidney, and effectively protected the kidney function in
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