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

[81] HSPB1, HSPB6, HSPB7 and HSPB8 Protect against RhoA GTPase-Induced Remodeling in Tachypaced Atrial Myocytes [J].

Ke, Lei ;

Meijering, Roelien A. M. ;

Hoogstra-Berends, Femke ;

Mackovicova, Katarina ;

Vos, Michel J. ;

Van Gelder, Isabelle C. ;

Henning, Robert H. ;

Kampinga, Harm H. ;

Brundel, Bianca J. J. M. .

PLOS ONE, 2011, 6 (06)

[82] Oxidative stress-associated impairment of proteasome activity during ischemia-reperfusion injury [J].

Keller, JN ;

Huang, FF ;

Zhu, H ;

Yu, J ;

Ho, YS ;

Kindy, MS .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2000, 20 (10) :1467-1473

[83] Partially folded intermediates as critical precursors of light chain amyloid fibrils and amorphous aggregates [J].

Khurana, R ;

Gillespie, JR ;

Talapatra, A ;

Minert, LJ ;

Ionescu-Zanetti, C ;

Millett, I ;

Fink, AL .

BIOCHEMISTRY, 2001, 40 (12) :3525-3535

[84] Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities [J].

Kim, Inki ;

Xu, Wenjie ;

Reed, John C. .

NATURE REVIEWS DRUG DISCOVERY, 2008, 7 (12) :1013-1030

[85] Molecular Chaperone Functions in Protein Folding and Proteostasis [J].

Kim, Yujin E. ;

Hipp, Mark S. ;

Bracher, Andreas ;

Hayer-Hartl, Manajit ;

Hartl, F. Ulrich .

ANNUAL REVIEW OF BIOCHEMISTRY, VOL 82, 2013, 82 :323-355

[86] Myocytes die by multiple mechanisms in failing human hearts [J].

Kostin, S ;

Pool, L ;

Elsässer, A ;

Hein, S ;

Drexler, HCA ;

Arnon, E ;

Hayakawa, Y ;

Zimmermann, R ;

Bauer, E ;

Klövekorn, WP ;

Schaper, J .

CIRCULATION RESEARCH, 2003, 92 (07) :715-724

[87] Selective autophagy: ubiquitin-mediated recognition and beyond [J].

Kraft, Claudine ;

Peter, Matthias ;

Hofmann, Kay .

NATURE CELL BIOLOGY, 2010, 12 (09) :836-841

[88] Heat shock protein 90 transfection reduces ischemia-reperfusion-induced myocardial dysfunction via reciprocal endothelial NO synthase serine 1177 phosphorylation and threonine 495 dephosphorylation [J].

Kupatt, C ;

Dessy, C ;

Hinkel, R ;

Raake, P ;

Daneau, G ;

Bouzin, C ;

Boekstegers, P ;

Feron, O .

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (08) :1435-1441

[89] The Biology of Proteostasis in Aging and Disease [J].

Labbadia, Johnathan ;

Morimoto, Richard I. .

ANNUAL REVIEW OF BIOCHEMISTRY, VOL 84, 2015, 84 :435-464

[90]

Lamark T., 2012, International Journal of Cell Biology

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