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Kai Wang

Researcher at Cleveland Clinic

Publications -  21
Citations -  829

Kai Wang is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Internal medicine & Neointimal hyperplasia. The author has an hindex of 12, co-authored 16 publications receiving 800 citations.

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Receptor for AGE (RAGE) Mediates Neointimal Formation in Response to Arterial Injury

TL;DR: Findings indicate that RAGE/ligand interaction plays a key role in neointimal formation after vascular injury irrespective of diabetes status and suggest a novel target to minimize neointedimal hyperplasia.
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Increased Expression of Thrombospondin-1 in Vessel Wall of Diabetic Zucker Rat

TL;DR: Increased expression of TSP-1 in blood vessels in diabetes may represent a new link between diabetes, atherogenesis, and accelerated restenosis, and may be a direct response of vascular cells to glucose.
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Peroxisome proliferator-activated receptor gamma down-regulates receptor for advanced glycation end products and inhibits smooth muscle cell proliferation in a diabetic and nondiabetic rat carotid artery injury model.

TL;DR: It is demonstrated for the first time that PPARγ agonists inhibit RAGE expression at sites of arterial injury and suggest that down-regulation of RAGE by the PParγ activation inhibits neointimal formation in response to arterial Injury.
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Adjunctive treatment with ticagrelor, but not clopidogrel, added to tPA enables sustained coronary artery recanalisation with recovery of myocardium perfusion in a canine coronary thrombosis model.

TL;DR: Ticagrelor blocks ADP-induced platelet activation and aggregation; prevents platelet-mediated thrombosis; prolongs reperfusion time and reduces re-occlusion and cyclic flow variation; and significantly decreases infarct size and rapidly restores myocardial tissue perfusion.
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Blockade of the Platelet P2Y12 Receptor by AR-C69931MX Sustains Coronary Artery Recanalization and Improves the Myocardial Tissue Perfusion in a Canine Thrombosis Model

TL;DR: The adjunctive administration of AR-C69931MX blocked ADP-mediated platelet aggregation and recruitment and prevented platelet-mediated thrombosis, resulting in prolongation of reperfusion time and a decrease in reocclusion and cyclic flow variations.