YY1 nitration participates in DbCM cardiomyocyte lipotoxicity by inhibiting ANXA3-induced microlipophagy
T2DM promoted cardiomyocyte YY1 nitration at Y<sup>185</sup> and Y<sup>383</sup> residues. Y<sup>185</sup> site nitration inhibited YY1 nuclear translocation, thereby attenuating ANXA3 transcription. Microlipophagy emerged as the principal lipid droplet degradation mechanism in diabetic cardiomyocytes. ANXA3 downregulation suppresses Rab7a expression, impairing microlipophagy and causing lipid deposition that exacerbates DbCM progression. Therapeutic strategies targeting YY1 nitration inhibition or enhancing ANXA3-mediated microlipophagy demonstrate therapeutic potential for mitigating.
Authors
- Jiayin Chai (ORCID: https://orcid.org/0000-0001-5146-0080)
- Yuqing Ding (ORCID: https://orcid.org/0000-0003-3915-7542)
- Lijie Han
- S W Chen
- Y H Bai
- Xuetao Zhu (ORCID: https://orcid.org/0000-0002-7563-1603)
- Degang Mo
- Xiangning Kong
- Yiming Yang
- Lijia Xu
- Wen Wang
- Hongyan Dai
Institutions
- Qingdao University (CN)
- Capital Medical University (CN)
- Capital Institute of Pediatrics (CN)
- Qingdao Municipal Hospital (CN)
Publication Details
- Journal
- Redox Biology
- Published
- 2026-02-12
- DOI
- https://doi.org/10.1016/j.redox.2026.104085
- Primary Topic
- Cardiovascular Function and Risk Factors
- Type
- article
- Field-Weighted Citation Impact
- 0.00