Abstract
Developing endothelial-protective, nonthrombogenic antirestenotic treatments has been a challenge. A major hurdle to this has been the identification of a common molecular target in both smooth muscle cells and endothelial cells, inhibition of which blocks dysfunction of both cell types. The authors’ findings suggest that the PERK kinase could be such a target. Importantly, PERK inhibition mitigated both restenosis and thrombosis in preclinical models, implicating a low-thrombogenic antirestenotic paradigm.
| Original language | English |
|---|---|
| Pages (from-to) | 245-263 |
| Number of pages | 19 |
| Journal | JACC: Basic to Translational Science |
| Volume | 5 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 2020 |
Bibliographical note
Publisher Copyright:© 2020 The Authors
Funding
This work was supported by National Institutes of Health grants R01HL143469, R01HL129785 (to Drs. Gong, Guo, and Kent), R01HL133665 (to Dr. Guo), K25CA166178 (to Dr. Gong), and American Heart Association pre-doctoral awards 17PRE33670865 (to Dr. Zhang) and 16PRE30160010 (to Dr. Wang). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
| Funders | Funder number |
|---|---|
| National Institutes of Health (NIH) | R01HL129785, K25CA166178, R01HL143469 |
| National Heart, Lung, and Blood Institute (NHLBI) | R01HL133665 |
| American the American Heart Association | 16PRE30160010, 17PRE33670865 |
Keywords
- PERK
- endothelial cells
- restenosis
- smooth muscle cells
- thrombosis
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
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