PERK inhibition mitigates restenosis and thrombosis: a potential low-thrombogenic antirestenotic paradigm
Basic to Translational Science, 2020•jacc.org
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.
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.
Summary
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.
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