Salazar Juan, Martínez María Sofía, Chávez-Castillo Mervin, Núñez Victoria, Añez Roberto, Torres Yaquelin, Toledo Alexandra, Chacín Maricarmen, Silva Carlos, Pacheco Enrique, Rojas Joselyn, Bermúdez Valmore
Endocrine and Metabolic Diseases Research Center, School of Medicine, Zulia University, 20th Avenue, Maracaibo 4004, Venezuela.
Endocrine and Metabolic Diseases Research Center, School of Medicine, Zulia University, 20th Avenue, Maracaibo 4004, Venezuela; Institute of Clinical Immunology, University of Los Andes, Mérida 5101, Mérida, Venezuela.
Int Sch Res Notices. 2014 Dec 15;2014:653045. doi: 10.1155/2014/653045. eCollection 2014.
Cardiovascular disease is the leading cause of morbidity and mortality in the adult population worldwide, with atherosclerosis being its key pathophysiologic component. Atherosclerosis possesses a fundamental chronic inflammatory aspect, and the involvement of numerous inflammatory molecules has been studied in this scenario, particularly C-reactive protein (CRP). CRP is a plasma protein with strong phylogenetic conservation and high resistance to proteolysis, predominantly synthesized in the liver in response to proinflammatory cytokines, especially IL-6, IL-1β, and TNF. CRP may intervene in atherosclerosis by directly activating the complement system and inducing apoptosis, vascular cell activation, monocyte recruitment, lipid accumulation, and thrombosis, among other actions. Moreover, CRP can dissociate in peripheral tissue-including atheromatous plaques-from its native pentameric form into a monomeric form, which may also be synthesized de novo in extrahepatic sites. Each form exhibits distinct affinities for ligands and receptors, and exerts different effects in the progression of atherosclerosis. In view of epidemiologic evidence associating high CRP levels with cardiovascular risk-reflecting the biologic impact it bears on atherosclerosis-measurement of serum levels of high-sensitivity CRP has been proposed as a tool for assessment of cardiovascular risk.
心血管疾病是全球成年人群发病和死亡的主要原因，动脉粥样硬化是其关键的病理生理组成部分。动脉粥样硬化具有基本的慢性炎症特征，在这种情况下，人们对多种炎症分子的参与进行了研究，特别是C反应蛋白（CRP）。CRP是一种血浆蛋白，具有很强的系统发育保守性和对蛋白水解的高抗性，主要在肝脏中合成，以响应促炎细胞因子，尤其是白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子（TNF）。CRP可能通过直接激活补体系统、诱导细胞凋亡、血管细胞活化、单核细胞募集、脂质积聚和血栓形成等作用来干预动脉粥样硬化。此外，CRP可以在包括动脉粥样斑块在内的外周组织中从其天然的五聚体形式解离为单体形式，单体形式也可能在肝外部位重新合成。每种形式对配体和受体表现出不同的亲和力，并在动脉粥样硬化的进展中发挥不同的作用。鉴于流行病学证据表明高CRP水平与心血管风险相关——反映了其对动脉粥样硬化的生物学影响——高敏CRP血清水平的测量已被提议作为评估心血管风险的一种工具。
