Head Trajen, Daunert Sylvia, Goldschmidt-Clermont Pascal J
Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL, United States.
Division of Cardiology, University of Miami Miller School of Medicine, Miami, FL, United States.
Front Genet. 2017 Dec 14;8:216. doi: 10.3389/fgene.2017.00216. eCollection 2017.
A considerable volume of research over the last decade has focused on understanding the fundamental mechanisms for the progression of atherosclerosis-the underlying cause for the vast majority of all cardiovascular (CVD)-related complications. Aging is the dominant risk factor for clinically significant atherosclerotic lesion formation, yet the heightened impact of aging on the disease is not accounted for by changes in traditional risk factors, such as lack of physical activity, smoking, hypertension, hyperlipidemia, or diabetes mellitus. This review will examine the pathological and biochemical processes of atherosclerotic plaque formation and growth, with particular focus on the aging risk vis-a-vis arterial homeostasis. Particular focus will be placed on the impact of a number of important contributors to arterial homeostasis including bone marrow (BM)-derived vascular progenitor cells, differential monocyte subpopulations, and the role of cellular senescence. Finally, this review will explore many critical observations in the way the disease process has been reassessed both by clinicians and researchers, and will highlight recent advances in this field that have provided a greater understanding of this aging-driven disease.
在过去十年中,大量研究致力于了解动脉粥样硬化进展的基本机制,而动脉粥样硬化是绝大多数心血管疾病(CVD)相关并发症的根本原因。衰老 是临床上显著的动脉粥样硬化病变形成的主要风险因素,然而,衰老对该疾病的影响加剧,并非由缺乏体育活动、吸烟、高血压、高脂血症或糖尿病等传统风险因素的变化所导致。本综述将研究动脉粥样硬化斑块形成和生长的病理及生化过程,特别关注衰老对动脉稳态的风险。将特别关注一些对动脉稳态有重要贡献的因素的影响,包括骨髓(BM)来源的血管祖细胞、不同的单核细胞亚群以及细胞衰老的作用。最后,本综述将探讨临床医生和研究人员重新评估疾病过程的许多关键观察结果,并强调该领域的最新进展,这些进展使人们对这种由衰老驱动的疾病有了更深入的了解。