FOXO1 Integrates Endothelial Hemodynamic, Inflammatory, and Metabolic Pathways in Atherosclerosis
These findings identify FOXO1 as a key mediator linking atheroprone flow and endothelial inflammatory gene expression via lactate-driven lactylation and nuclear translocation, promoting atherosclerosis. Conversely, physiological FSS suppresses FOXO1 via KLF2-CDK2 signaling. These complementary pathways suggest potential new therapeutic targets for treating atherosclerotic cardiovascular disease.
Authors
- Hanqiang Deng (ORCID: https://orcid.org/0000-0001-5976-517X)
- Yewei Wang (ORCID: https://orcid.org/0000-0002-2213-5198)
- Divyesh Joshi (ORCID: https://orcid.org/0000-0002-4415-2677)
- George Tellides (ORCID: https://orcid.org/0000-0001-7042-8190)
- Xing Zhang (ORCID: https://orcid.org/0000-0002-2925-224X)
Institutions
- Emory University (US)
- Yale University (US)
- Cardiovascular Research Center (BR)
Publication Details
- Journal
- Circulation Research
- Published
- 2026-02-25
- DOI
- https://doi.org/10.1161/circresaha.125.327592
- Citations
- 1
- Primary Topic
- FOXO transcription factor regulation
- Type
- article
- Field-Weighted Citation Impact
- 22.24