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atherosclerotic plaque progression and instability

With the development of atherosclerotic lesion, new vessels sprouting from the adventitia neovascularize the growing plaque. Inflammatory cells could be recruited through neovascularization, leading to exacerbation of inflammatory state and acceleration of plaque growth [ even in-stent restenosis (ISR) [Plaque neovascularization is thought to contribute to the plaque instability, and ultimately results in thromboembolic complications Therefore, the functional roles of TRPCs in neovascularization have received great attention in recent yearsPrevious studies have suggested that TRPC6 plays key roles in growth-factor-induced angiogenesis during plaque neovascularization In addition to TRPC6, TRPC4 has recently been attracting increased research attention. TRPC4, an essential component of the nonselective calcium-permeable cation channel, is assumed to be activated by Gq/phospholipase C-coupled receptors and tyrosine kinasesand it is associated with multiple processes, including cell proliferation, endothelial permeability, vasodilation, and neurotransmitter releaseSong et al. confirmed that suppression of TPRC4 inhibits retinal neovascularization Given the multiple functions of TPRC4, we hypothesized that TPRC4 might play a critical role in angiogenesis involved in atherosclerosis.