Dynamic changes in chromatin accessibility are associated with the atherogenic transitioning of vascular smooth muscle cells.
Ying WangHua GaoFudi WangZhongde YeMichal MokryAdam W TurnerJianqin YeSimon KoplevLingfeng LuoTom AlsaighShaunak S AdkarMaria ElishaevXiangyu GaoLars MaegdefesselJohan L M BjörkegrenGerard PasterkampClint L MillerElsie G RossNicholas J LeeperPublished in: Cardiovascular research (2021)
The recent CANTOS and COLCOT trials have shown that targeting inflammatory pathways lowers the risk of major adverse cardiovascular events. However, more specific targets are needed to avoid immunosuppressive side effects. Our data identify an upstream regulator of pro-inflammatory SMCs, ATF3, which is involved in the initial atherogenic transitioning of lesional SMCs. Restoring ATF3 activity may prevent the de-differentiation of SMCs and offer a novel translational approach for the suppression of complement-dependent inflammation in atherosclerotic lesions.
Keyphrases
- cardiovascular events
- vascular smooth muscle cells
- transcription factor
- oxidative stress
- coronary artery disease
- angiotensin ii
- cardiovascular disease
- endoplasmic reticulum stress
- dna damage
- electronic health record
- low density lipoprotein
- genome wide
- cancer therapy
- gene expression
- emergency department
- data analysis
- adverse drug