ArticleEMBO molecular medicine2021
Pdia4 regulates β-cell pathogenesis in diabetes: molecular mechanism and targeted therapy.
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Polyadenylation of insulin mRNA by Tent5a regulates pancreatic beta cells.Nature communications · 2026Article
- Homoharringtonine inhibits growth and migration in non-small cell lung cancer via PDIA4-mediated modulation of autophagy and EMT.Archives of pharmacal research · 2026Article
- Defects inFrontiers in genetics · 2026Article
- Antimicrobial peptide CRAMP/LL-37 mediates ferroptosis resistance in cardiomyocytes by inhibiting cathepsin L.Basic research in cardiology · 2025Article
- AMPK pathway: an emerging target to control diabetes mellitus and its related complications.Journal of diabetes and metabolic disorders · 2024Review
- Article
- Pharmacological and mechanistic study of PS1, a Pdia4 inhibitor, in β-cell pathogenesis and diabetes in db/db mice.Cellular and molecular life sciences : CMLS · 2023Article
- Construction and validation of a cuproptosis-related prognostic model for glioblastoma.Frontiers in immunology · 2023Article
- Protein Disulfide Isomerases Function as the Missing Link Between Diabetes and Cancer.Antioxidants & redox signaling · 2022Review
- The Role of Obesity and Diabetes in Dementia.International journal of molecular sciences · 2022Review
- PDIA4, a new endoplasmic reticulum stress protein, modulates insulin resistance and inflammation in skeletal muscle.Frontiers in endocrinology · 2022Article
- Pdia4 regulates β-cell pathogenesis in diabetes: molecular mechanism and targeted therapy.EMBO molecular medicine · 2021Article
Corrections and comments
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Authors and funding
16 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of β-cell number and function is a hallmark of diabetes. β-cell preservation is emerging as a promising strategy to treat and reverse diabetes. Here, we first found that Pdia4 was primarily expressed in β-cells. This expression was up-regulated in β-cells and blood of mice in response to excess nutrients. Ablation of Pdia4 alleviated diabetes as shown by reduced islet destruction, blood glucose and HbA1c, reactive oxygen species (ROS), and increased insulin secretion in diabetic mice. Strikingly, this ablation alone or in combination with food reduction could fully reverse diabetes. Conversely, overexpression of Pdia4 had the opposite pathophysiological outcomes in the mice. In addition, Pdia4 positively regulated β-cell death, dysfunction, and ROS production. Mechanistic studies demonstrated that Pdia4 increased ROS content in β-cells via its action on the pathway of Ndufs3 and p22
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