Protein aggregation, cardiovascular diseases, and exercise training: Where do we stand?

被引：50

作者：

Gouveia, Marisol ^{[1
,2
]}

Xia, Ke ^{[3
]}

Colon, Wilfredo ^{[3
]}

Vieira, Sandra I. ^{[1
,2
]}

Ribeiro, Fernando ^{[2
,4
]}

机构：

[1] Univ Aveiro, Dept Med Sci, Aveiro, Portugal

[2] Univ Aveiro, Inst Biomed iBiMED, Aveiro, Portugal

[3] Rensselaer Polytech Inst, Dept Chem & Chem Biol, Ctr Biotechnol & Interdisciplinary Studies, Troy, NY USA

[4] Univ Aveiro, Sch Hlth Sci, Bldg 30,Campus Univ Santiago, P-3810193 Aveiro, Portugal

来源：

AGEING RESEARCH REVIEWS | 2017年 / 40卷

关键词：

Protein aggregation; Proteostasis; Aging; Cardiovascular diseases; Exercise; UBIQUITIN-PROTEASOME SYSTEM; ENDOPLASMIC-RETICULUM STRESS; ALPHA-B-CRYSTALLIN; CORONARY-ARTERY-DISEASE; CHAIN AMYLOID FIBRILS; HEAT-SHOCK PROTEINS; QUALITY-CONTROL; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; TRANSGENIC MICE;

D O I：

10.1016/j.arr.2017.07.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cells ensure their protein quality control through the proteostasis network. Aging and age-related diseases, such as neurodegenerative and cardiovascular diseases, have been associated to the reduction of proteostasis network efficiency and, consequently, to the accumulation of protein misfolded aggregates. The decline in protein homeostasis has been associated with the development and progression of atherosclerotic cardiovascular disease, cardiac hypertrophy, cardiomyopathies, and heart failure. Exercise training is a key component of the management of patients with cardiovascular disease, consistently improving quality of life and prognosis. In this review, we give an overview on age-related protein aggregation, the role of the increase of misfolded protein aggregates on cardiovascular pathophysiology, and describe the beneficial or deleterious effects of the proteostasis network on the development of cardiovascular disease. We subsequently discuss how exercise training, a key lifestyle intervention in those with cardiovascular disease, could restore proteostasis and improve disease status. (C) 2017 Elsevier B.V. All rights reserved.

引用

页码：1 / 10

页数：10

共 192 条

[41] Targeting the Ubiquitin-Proteasome System in Heart Disease: The Basis for New Therapeutic Strategies [J].

Drews, Oliver ;

Taegtmeyer, Heinrich .

ANTIOXIDANTS & REDOX SIGNALING, 2014, 21 (17) :2322-2343

[42] Distinct Roles In Vivo for the Ubiquitin-Proteasome System and the Autophagy-Lysosomal Pathway in the Degradation of α-Synuclein [J].

Ebrahimi-Fakhari, Darius ;

Cantuti-Castelvetri, Ippolita ;

Fan, Zhanyun ;

Rockenstein, Edward ;

Masliah, Eliezer ;

Hyman, Bradley T. ;

McLean, Pamela J. ;

Unni, Vivek K. .

JOURNAL OF NEUROSCIENCE, 2011, 31 (41) :14508-14520

[43] Effects of the mutations Ala30 to Pro and Ala53 to Thr on the physical and morphological properties of α-synuclein protein implicated in Parkinson's disease [J].

El-Agnaf, OMA ;

Jakes, R ;

Curran, MD ;

Wallace, A .

FEBS LETTERS, 1998, 440 (1-2) :67-70

[44] Novel cardioprotective role of a small heat-shock protein, Hsp20, against ischemia/reperfusion injury [J].

Fan, GC ;

Ren, XP ;

Qian, J ;

Yuan, QY ;

Nicolaou, P ;

Wang, Y ;

Jones, WK ;

Chu, GX ;

Kranias, EG .

CIRCULATION, 2005, 111 (14) :1792-1799

[45] The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages [J].

Feng, B ;

Yao, PM ;

Li, YK ;

Devlin, CM ;

Zhang, DJ ;

Harding, HP ;

Sweeney, M ;

Rong, JX ;

Kuriakose, G ;

Fisher, EA ;

Marks, AR ;

Ron, D ;

Tabas, I .

NATURE CELL BIOLOGY, 2003, 5 (09) :781-792

[46] The action of molecular chaperones in the early secretory pathway [J].

Fewell, SW ;

Travers, KJ ;

Weissman, JS ;

Brodsky, JL .

ANNUAL REVIEW OF GENETICS, 2001, 35 :149-191

[47] Unfolded Protein Response Regulates Cardiac Sodium Current in Systolic Human Heart Failure [J].

Gao, Ge ;

Xie, An ;

Zhang, Jianhua ;

Herman, Amanda M. ;

Jeong, Euy-Myoung ;

Gu, Lianzhi ;

Liu, Man ;

Yang, Kai-Chien ;

Kamp, Timothy J. ;

Dudley, Samuel C. .

CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY, 2013, 6 (05) :1018-1024

[48] Glucose deprivation induces reticulum stress by the PERK pathway and caspase-7-and calpain-mediated caspase-12 activation [J].

Garcia de la Cadena, Selene ;

Hernandez-Fonseca, Karla ;

Camacho-Arroyo, Ignacio ;

Massieu, Lourdes .

APOPTOSIS, 2014, 19 (03) :414-427

[49] Impaired cardiac autophagy in patients developing postoperative atrial fibrillation [J].

Garcia, Lorena ;

Verdejo, Hugo E. ;

Kuzmicic, Jovan ;

Zalaquett, Ricardo ;

Gonzalez, Sergio ;

Lavandero, Sergio ;

Corbalan, Ramon .

JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 2012, 143 (02) :451-U485

[50]

Gielen S, 2001, CIRCULATION, V103, pE1

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