Recent Progress in Vascular Aging: Mechanisms and Its Role in Age-related Diseases

被引:55
作者
Xu, Xianglai [1 ,2 ]
Wang, Brian [2 ]
Ren, Changhong [2 ,4 ]
Hu, Jiangnan [2 ]
Greenberg, David A. [5 ]
Chen, Tianxiang [6 ]
Xie, Liping [3 ]
Jin, Kunlin [2 ]
机构
[1] Fudan Univ, Zhongshan Hosp, Shanghai 200032, Peoples R China
[2] Univ North Texas, Hlth Sci Ctr, Dept Pharmacol & Neurosci, Ft Worth, TX 76107 USA
[3] Zhejiang Univ, Affiliated Hosp 1, Dept Urol, Hangzhou, Zhejiang, Peoples R China
[4] Capital Med Univ, Xuanwu Hosp, Inst Hypoxia Med, Beijing, Peoples R China
[5] Buck Inst Res Aging, Novato, CA 94945 USA
[6] Shanghai Jiao Tong Univ, Shanghai Chest Hosp, Dept Thorac Surg, Shanghai, Peoples R China
来源
AGING AND DISEASE | 2017年 / 8卷 / 04期
基金
美国国家卫生研究院; 美国国家科学基金会; 中国国家自然科学基金;
关键词
vascular aging; stroke; dementia; arterial stiffness; endothelial dysfunction; SMALL VESSEL DISEASE; CEREBRAL-BLOOD-FLOW; MONOCYTE CHEMOATTRACTANT PROTEIN-1; SMOOTH-MUSCLE-CELLS; PULSE-WAVE VELOCITY; MITOCHONDRIAL-DNA DELETIONS; TESTOSTERONE REPLACEMENT THERAPY; MILD COGNITIVE IMPAIRMENT; RENIN-ANGIOTENSIN SYSTEM; TRANSGENIC MOUSE MODEL;
D O I
10.14336/AD.2017.0507
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
As with many age-related diseases including vascular dysfunction, age is considered an independent and crucial risk factor. Complicated alterations of structure and function in the vasculature are linked with aging hence, understanding the underlying mechanisms of age-induced vascular pathophysiological changes holds possibilities for developing clinical diagnostic methods and new therapeutic strategies. Here, we discuss the underlying molecular mediators that could be involved in vascular aging, e.g., the renin-angiotensin system and pro-inflammatory factors, metalloproteinases, calpain-1, monocyte chemoattractant protein-1 (MCP-1) and TGF beta-1 as well as the potential roles of testosterone and estrogen. We then relate all of these to clinical manifestations such as vascular dementia and stroke in addition to reviewing the existing clinical measurements and potential interventions for age-related vascular dysfunction.
引用
收藏
页码:486 / 505
页数:20
相关论文
共 212 条
[1]   Lactadherin deficiency leads to apoptotic cell accumulation and accelerated atherosclerosis in mice [J].
Ait-Oufella, Hafid ;
Kinugawa, Kiyoka ;
Zoll, Joffrey ;
Simon, Tabassome ;
Boddaert, Jacques ;
Heeneman, Silvia ;
Blanc-Brude, Olivier ;
Barateau, Veronique ;
Potteaux, Stephane ;
Merval, Regine ;
Esposito, Bruno ;
Teissier, Elisabeth ;
Daemen, Mat J. ;
Leseche, Guy ;
Boulanger, Chantal ;
Tedgui, Alain ;
Mallat, Ziad .
CIRCULATION, 2007, 115 (16) :2168-2177
[2]  
Akinyemi RO, 2013, CURR ALZHEIMER RES, V10, P642
[3]   Low testosterone level is an independent determinant of endothelial dysfunction in men [J].
Akishita, Masahiro ;
Hashimoto, Masayoshi ;
Ohike, Yurniko ;
Ogawa, Surnito ;
Iijima, Katsuya ;
Eto, Masato ;
Ouchi, Yasuyoshi .
HYPERTENSION RESEARCH, 2007, 30 (11) :1029-1034
[4]   Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: Implication in the pathogenesis of Alzheimer's disease [J].
Aliev, Gjumrakch ;
Gasimov, Eldar ;
Obrenovich, Mark E. ;
Fischbach, Kathryn ;
Shenk, Justin C. ;
Smith, Mark A. ;
Perry, George .
VASCULAR HEALTH AND RISK MANAGEMENT, 2008, 4 (03) :721-730
[5]  
[Anonymous], COCHRANE DATABASE SY
[6]  
[Anonymous], J CLIN NEUROSCI
[7]   MFG-E8 inhibits neutrophil migration through αvβ3-integrin-dependent MAP kinase activation [J].
Aziz, Monowar ;
Yang, Weng-Lang ;
Corbo, Lana M. ;
Chaung, Wayne W. ;
Matsuo, Shingo ;
Wang, Ping .
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 2015, 36 (01) :18-28
[8]   Huntington's disease and mitochondrial DNA deletions: Event or regular mechanism for mutant Huntingtin protein and CAG repeats expansion?! [J].
Banoei, Mohammad Mehdi ;
Houshmand, Massoud ;
Panahi, Mehdi Shafa Shariat ;
Shariati, Parvin ;
Rostami, Maryam ;
Manshadi, Masoumeh Dehghan ;
Majidizadeh, Tayebeh .
CELLULAR AND MOLECULAR NEUROBIOLOGY, 2007, 27 (07) :867-875
[9]   Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals [J].
Barja, G ;
Herrero, A .
FASEB JOURNAL, 2000, 14 (02) :312-318
[10]   Protective effect of long-term angiotensin II inhibition [J].
Basso, Nidia ;
Cini, Rosa ;
Pietrelli, Adriana ;
Ferder, Leon ;
Terragno, Norberto A. ;
Inserra, Felipe .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2007, 293 (03) :H1351-H1358