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©The Author(s) 2025.
World J Diabetes. Apr 15, 2025; 16(4): 104241
Published online Apr 15, 2025. doi: 10.4239/wjd.v16.i4.104241
Published online Apr 15, 2025. doi: 10.4239/wjd.v16.i4.104241
Figure 1 The effects of Plantamajoside on pancreatic β-cells in type 2 diabetes mellitus.
Upregulation of DNAJC1 results in the suppression of endoplasmic reticulum (ER) stress markers such as CHOP and β-cell apoptosis[29]. ERK and NF-κB regulate both pro-apoptotic and anti-apoptotic effects, depending on the stimulus and the cell type. The ER stress marker CHOP stimulates the intrinsic apoptotic pathway by inhibiting the antiapoptotic protein Bcl-2. Bcl-2 inhibition by CHOP releases the autophagy protein Beclin-1 from the Bcl-2-Beclin1 complex, allowing Beclin-1 to initiate autophagy via the formation of isolation (autophagosomal) membrane. Thus, Plantamajoside may inhibit apoptosis and activate autophagy in stressed β-cells as a pro-survival mechanism[3,5,23,26,27,32-34].
- Citation: Al-Bari MAA, Davamani F, Bhatnagar P, Eid N. Plantamajoside mitigates endoplasmic reticulum stress-mediated pancreatic β-cell apoptosis in type 2 diabetes via DNAJC1 upregulation. World J Diabetes 2025; 16(4): 104241
- URL: https://www.wjgnet.com/1948-9358/full/v16/i4/104241.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i4.104241