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Synthetic DNA-Based Compounds for the Prevention of Coronary Restenosis: Current Status and Future Challenges
Published in Eric Wickstrom, Clinical Trials of Genetic Therapy with Antisense DNA and DNA Vectors, 2020
Andrew Zalewski, Yi Shi, John D. Mannion, Femando Roqué
A rapid release of growth factors and cytokines from platelets and cell debris at the site of transcatheter interventions sets the conditions for paracrine and autocrine stimulation of resident cells in the arterial wall. This ultimately leads to the formation of neointima, which differs from atherosclerotic plaque or normal vessel wall (Ross et al., 1984). Its primary function is to repair the injured tissue (e.g., fill dissection in the media), although often neointimal formation is excessive and may contribute to restenosis (Figure IB).
The protective effect of tanshinone IIa on endothelial cells: a generalist among clinical therapeutics
Published in Expert Review of Clinical Pharmacology, 2021
Jun Feng, Lina Liu, Fangfang Yao, Daixing Zhou, Yang He, Junshuai Wang
Atherosclerosis is a multifactorial and multistage chronic inflammatory disease characterized by an inflammatory response, oxidative stress, and immune disorders. There are several sequential and correlated stages in the development of atherosclerosis, among which endothelial dysfunction plays a critical role. The combination of multiple pro-atherogenic factors, especially oxidized low-density lipoprotein (LDL), high glucose, and homocysteine, destroys the integrity of the vascular endothelial cell junctions, induces leaky vessels, and increases leukocyte (monocyte and neutrophil) adhesion to injured endothelial cells, impairs vasorelaxation, causes the uncoupling of endothelial nitric oxide synthase (eNOS), and decreases NO production [13,14]. The injured vascular endothelial cells subsequently induce the vascular smooth muscle cells to switch phenotype, proliferate, and migrate from the media layer of blood vessels to shape the neointima (or hyperplasia), the early stage of atherosclerosis. After disruption of atherosclerotic plaque, the plaque is susceptible to fracture, resulting in platelet activation (adhesion and aggregation), and thrombosis formation, which underlie the clinical pathophysiology of atherothrombotic events [15–17]. It is noteworthy that recent studies have demonstrated that mental stress is an important factor in the generation of pathophysiological sequelae in many disease conditions [18,19]. Stress hormones, including pro-inflammatory cytokines and glucocorticoids in response to mental stress, participate in endothelial dysfunction probably through the downregulation of eNOS expression, eNO inactivation, decreased NO actions, and increased NO degradation, combined with vasoconstriction against NO-induced vasodilatation [20–22]. These data proved the critical role of endothelial cells in maintaining physiological homeostasis and the final common pathway of atherosclerosis.