ArticleFrontiers in cell and developmental biology2025
Cdk5 mediates impaired autophagy by regulating NGF/Sirt1 axis to cause diabetic islet β cell damage.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Unveiling the TrkA-p35/CDK5 axis: a novel therapeutic target in diabetic kidney disease.Frontiers in endocrinology · 2026Article
- Nerve Growth Factor in Diabetes Mellitus: Pathophysiological Mechanisms, Biomarkers and Therapeutic Opportunities.Pharmaceuticals (Basel, Switzerland) · 2025Review
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9 authors.
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Abstract
The number of patients with diabetes is increasing annually, and islet β cell damage plays a central role in the occurrence and development of diabetes. The activation of cyclin-dependent kinase 5 (Cdk5) is involved in the development of diabetes; however, its specific mechanism has not been fully elucidated. This study aimed to investigate the role of Cdk5 in diabetic islet β cell injury. Our results indicate that Cdk5 is upregulated in islet β cells under diabetic conditions, which results in impaired autophagy, and that its inhibition mitites islet β cell injury. In addition, high glucose decreased the levels of nerve growth factor (NGF) and Sirtuin 1 (Sirt1). NGF knockdown was associated with Sirt1 downregulation, while its overexpression upregulated Sirt1, restored autophagy, indicating that NGF positively regulates Sirt1 in islet β cells. Finally, we found that the NGF inhibitor K252a attenuated the protective effect of Lv-Cdk5 shRNA against high glucose-induced islet β cell injury in a mouse model. In conclusion, Cdk5 negatively regulates the NGF/Sirt1 axis, resulting in impaired autophagy of islet β cells under high glucose environments, which lead to islet β cell dysfunction. The Cdk5-NGF/Sirt1 axis may be a new target for the treatment of diabetes.
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