Hepatic–vascular crosstalk via GRK2: fenofibrate improves endothelial function by restoring lipid metabolism and NO signaling in obese mice
Fenofibrate improves endothelial-dependent relaxation and NO production in HFD-induced obese mice, likely through activation of the LKB1/AMPK/Akt pathway. The suppression of hepatic GRK2 activity by fenofibrate may contribute to better lipid metabolism, thereby promoting the recovery of vascular function.
Authors
- Tsuneo Kobayashi (ORCID: https://orcid.org/0000-0003-2758-0730)
- T. Furukawa (ORCID: https://orcid.org/0000-0001-5402-0777)
- Takayuki Matsumoto
- Haruka Yonaiyama
- Kumiko Taguchi
Institutions
- Kyushu University of Health and Welfare (JP)
- Kyushu University (JP)
- Hoshi University (JP)
Publication Details
- Journal
- Frontiers in Physiology
- Published
- 2026-01-12
- DOI
- https://doi.org/10.3389/fphys.2025.1734746
- Primary Topic
- Peroxisome Proliferator-Activated Receptors
- Type
- article
- Field-Weighted Citation Impact
- 0.00