Morphological and Molecular-Biological Changes in the Coronary Arteries after Stenting

Abstract

This review addresses morphological changes in coronary arteries following stenting, which result from damage to the vascular wall. These changes include 1) formation of a thrombus in the site of intimal injury; 2) inflammation; 3) proliferation and migration of smooth muscle cells; 4) formation of extracellular matrix. Each of these pathological processes has specific morpho-biological features. The review shows the role of von Willebrand factor in development of early thrombosis after intimal injury, which provokes activation of the inflammatory response followed by proliferation of smooth muscle cell that synthetize the extracellular matrix. These cellular and intercellular changes are based on overexpression of TGF-β1 protein, which facilitates modulation of various types of smooth muscle cells, including contractile and secretory ones. Issues of fine regulation of cellular and intercellular interactions by apoptosis, activation of mTOR signaling molecules, and microRNA are still understudied. Dynamic changes in drug-coated stents during development of neoatherosclerosis and late thrombosis remain not elucidated. Current reports show that initial mechanisms triggering pathological regenerative and hyperplastic processes that result in coronary restenosis in the area of implanted stents may form early (first hours or days) after stenting. Most studies were performed on experimental rather than on autopsy material, which does not allow fully unbiased interpretation of obtained data. Studying dynamics of morphological and molecular changes in coronary arteries after stenting, including on autopsy material, will allow one to express an opinion on the risk of postoperative thrombosis and restenosis.

Forensic (morphometric) characteristics of microcirculatory bloodstream vessels in fractures of lower limb segments

“…Во многом регуляция тонуса сосуда, изменение его диаметра определено функциональной активностью эндотелиальных клеток его внутреннего слоя, гемодинамическим напряжением сдвига и восприятием эндотелиальными клетками механического давления, которое оказывает движущаяся кровь (скорость кровотока) [14][15][16]. В настоящее время активно изучаются механизмы регуляции тонуса сосудов за счет механочувствительности эндотелиальных клеток [15,16]. Нарушение регуляции тонуса сосудов вносит существенный вклад в развитие различных патологических состояний, в том числе в процесс тромбообразования.…”