Copyright
©The Author(s) 2024.
World J Diabetes. Nov 15, 2024; 15(11): 2173-2176
Published online Nov 15, 2024. doi: 10.4239/wjd.v15.i11.2173
Published online Nov 15, 2024. doi: 10.4239/wjd.v15.i11.2173
Figure 1 Roles of NPAS2 and KANK1 in β-cell dysfunction in type 2 diabetes.
Figure depicts the key roles of NPAS2 and KANK1 in the dysfunction of pancreatic β-cells, a key event in the development of type 2 diabetes (T2D). The expression of NPAS2, a transcription factor, is upregulated in the islet β-cells of patients with T2D, leading to the upregulation of KANK1 expression. KANK1 disrupts the structural and functional integrity of β-cells by impairing cell adhesion and cytoskeletal dynamics. The interaction between NPAS2 and KANK1 contributes to β-cell apoptosis and impaired insulin secretion, thereby promoting the progression of T2D. This pathway highlights NPAS2 and KANK1 as potential therapeutic targets for preserving β-cell function and improving diabetes management.
- Citation: Cheng CH, Hao WR, Cheng TH. Targeting neuronal PAS domain protein 2 and KN motif/ankyrin repeat domains 1: Advances in type 2 diabetes therapy. World J Diabetes 2024; 15(11): 2173-2176
- URL: https://www.wjgnet.com/1948-9358/full/v15/i11/2173.htm
- DOI: https://dx.doi.org/10.4239/wjd.v15.i11.2173