title: Pathological mechanisms of erythrocyte-induced vulnerability of atherosclerotic plaques.
abstract: Erythrocytes are considered a new culprit contributing to atherosclerosis. Plaques with intraplaque hemorrhage are prone to new plaque hemorrhage, which may not only stimulate the progression of atherosclerosis but also promote the transition from a stable to an unstable lesion. However, the role of erythrocytes in inducing the vulnerability of plaque with intraplaque hemorrhage and the possible mechanism involved are not well understood. Recently, increased cholesterol level from erythrocytes was reported to expand the lipid core of plaque. As well, heme, iron and phospholipids derived from erythrocytes trigger peroxidization in vitro, which is strongly associated with the progression of atherosclerosis. We speculate that erythrocytes trapped in plaque may induce vulnerability of atherosclerotic plaques not only by accumulating lipids but also by promoting peroxidization within plaques, thereby expanding the lipid core, increasing the infiltration of inflammatory cells and attenuating the fibrous cap of plaques. This proposition may provide clues into the development of novel treatments to increase the stability of atherosclerotic plaques.
authors.affiliation: The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University Qilu Hospital, Jinan, Shandong 250012, China.
authors.forename: Hui-Li
authors.initials: HL
authors.lastname: Lin
authors.forename: Xin-sheng
authors.initials: XS
authors.lastname: Xu
authors.forename: Hui-xia
authors.initials: HX
authors.lastname: Lu
authors.forename: Chang-jiang
authors.initials: CJ
authors.lastname: Li
authors.forename: Meng-xiong
authors.initials: MX
authors.lastname: Tang
authors.forename: Hui-wen
authors.initials: HW
authors.lastname: Sun
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D050197:Atherosclerosis / Q000473:pathology*; D004912:Erythrocytes / Q000473:pathology / Q000502:physiology*; D006801:Humans; D058225:Plaque, Amyloid / Q000473:pathology