CASK mediates methylglyoxal-induced mitochondria-associated cell death in retinal Müller cells through modulating the ROS-p38-SOCE signalling pathway and antioxidant enzymes
accumulation and apoptosis. Transcriptomic analysis revealed that CASK silencing upregulated genes involved in mitochondrial respiration and oxidative phosphorylation, particularly complexes I and V. Collectively, these findings demonstrate that CASK promotes MGO-induced apoptosis through kinase-independent disruption of mitochondrial and antioxidant defenses, and kinase-dependent activation of SOCE, identifying CASK as a potential therapeutic target in DR.
Authors
- Ponarulselvam Sekar (ORCID: https://orcid.org/0000-0003-4282-2865)
- Liang Wu (ORCID: https://orcid.org/0000-0002-1907-411X)
- Wan‐Wan Lin (ORCID: https://orcid.org/0000-0002-3207-734X)
- Chuin Shung Yeoh
- Wan-Chen Huang
- Duen-Yi Huang
- Chi-Ming Chan
- Chieh-Ying Chen
Institutions
- Fu Jen Catholic University (TW)
- National Taiwan University (TW)
- Taipei Medical University Hospital (TW)
- Institute of Cellular and Organismic Biology, Academia Sinica (TW)
- Cardinal Tien Hospital (TW)
- Taipei Medical University (TW)
Publication Details
- Journal
- Biomedicine & Pharmacotherapy
- Published
- 2026-05-08
- DOI
- https://doi.org/10.1016/j.biopha.2026.119489
- Primary Topic
- Advanced Glycation End Products research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Science and Technology Council