The biology of restenosis
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Cited by (193)
Evaluation of Venous Stenosis Angioplasty in a Murine Arteriovenous Fistula Model
2019, Journal of Vascular and Interventional RadiologyLIM and cysteine-rich domains 1 is required for thrombininduced smooth muscle cell proliferation and promotes atherogenesis
2018, Journal of Biological ChemistryCitation Excerpt :Restenosis, characterized by arterial wall thickening and decreased arterial lumen space, occurs as a response to vascular injury (1, 2).
Endothelial Progenitor Cells: Properties, Function, and Response to Toxicological Stimuli
2018, Comprehensive Toxicology: Third EditionSoluble guanylyl cyclase-activated cyclic GMP-dependent protein kinase inhibits arterial smooth muscle cell migration independent of VASP-serine 239 phosphorylation
2016, Cellular SignallingCitation Excerpt :Because reactive oxygen species (ROS) are a risk factor for CVD pathologies, ROS-mediated oxidation of the sGC heme iron prevents NO binding and negatively impacts homeostatic cell signaling which has been found to promote aberrant ASM growth [5,6]. Additionally, current surgical strategies include balloon angioplasty and/or stent deployment which often fail due to vessel remodeling and neointimal development [7]. The current study was designed to investigate ability of pharmacologic heme-independent activation of endogenous sGC to prevent ASM cell migration as a key component of pathologic vascular growth.
Enhanced neointimal fibroblast, myofibroblast content and altered extracellular matrix composition: Implications in the progression of human peripheral artery restenosis
2016, AtherosclerosisCitation Excerpt :However, additional vascular cells may play a role in this proliferative process. Conventionally, resident intimal SMC proliferation plays a major role in restenosis [10]. SMCs include thin (α-actin positive) and thick (smooth muscle myosin heavy chain- SMMHC) filaments [11].