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PHACTR1, a coronary artery disease risk gene, mediates endothelial dysfunction
Xiaoxuan Ma1, Meiming Su1, Qingze He1
1Department of Endocrinology, Institute of Endocrine and Metabolic Diseases, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Clinical Research Hospital of Chinese Academy of Sciences (Hefei), University of Science and Technology of China, Hefei, China.
Frontiers in Immunology
|September 12, 2022
Summary
Phosphatase and actin regulator-1 (PHACTR1) promotes endothelial dysfunction and atherosclerosis by increasing inflammation and reducing nitric oxide. Targeting PHACTR1 may prevent polyvascular diseases.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Genetics
Background:
- Genome-wide association studies link PHACTR1 to polyvascular diseases.
- The role of PHACTR1 in endothelial dysfunction is not well understood.
Purpose of the Study:
- To investigate the role of PHACTR1 in endothelial dysfunction and atherosclerosis.
- To identify molecular mechanisms by which PHACTR1 affects endothelial cells.
Main Methods:
- Analysis of human plaque tissues and mouse models.
- RNA sequencing and cell biological studies.
- Proteomic analysis to identify interacting proteins.
Main Results:
- PHACTR1 is upregulated in vulnerable plaques and in mouse models of atherosclerosis.
- PHACTR1 overexpression disrupts endothelial homeostasis, promotes inflammation, and reduces nitric oxide production.
- PHACTR1 interacts with HSPA8 and influences ICAM1 and VCAM1 expression via NF-κB signaling.
Conclusions:
- PHACTR1 plays a deleterious role in endothelial function by inducing inflammation and reducing nitric oxide.
- Targeting PHACTR1 expression presents a potential therapeutic strategy for preventing endothelial dysfunction and atherosclerosis.
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