USP25 regulates atherosclerosis by restricting RIPK1-mediated inflammatory responses - PubMed
3 hours ago
- #Atherosclerosis
- #Inflammation
- #RIPK1
- USP25 is significantly downregulated in human atherosclerotic lesions.
- Ablation of macrophagic USP25 exacerbates atherosclerosis in ApoE-/- mice, increasing lipid deposition, macrophage infiltration, and vascular inflammation.
- USP25 inhibits inflammatory responses in macrophages by restricting the NF-κB pathway when stimulated with ox-LDL or TNF-α.
- RIPK1 is identified as a substrate of USP25, which removes K63 ubiquitin chains from RIPK1 via the C178 active site, attenuating RIPK1-mediated signal transduction.
- USP25 acts as a beneficial regulator in atherosclerosis by modulating RIPK1-mediated inflammatory responses.