Myocyte aging and mitochondrial turnover

被引：67

作者：

Terman, A ^{[1
]}

Brunk, UT ^{[1
]}

机构：

[1] Linkoping Univ, Fac Hlth Sci, Div Pathol 2, SE-58185 Linkoping, Sweden

来源：

EXPERIMENTAL GERONTOLOGY | 2004年 / 39卷 / 05期

关键词：

aging; autophagy; lysosomes; mitochondria; myocardium; oxidative stress; postmitotic cells; skeletal muscle;

D O I：

10.1016/j.exger.2004.01.005

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：

Cardiac myocytes, skeletal muscle fibers, and other long-lived postmitotic cells show dramatic age-related alterations that mainly affect mitochondria and the lysosomal compartment. Mitochondria are primary sites of reactive oxygen species formation that causes progressive damage to mitochondrial DNA and proteins in parallel to intralysosomal lipofuscin accumulation. There is amassing evidence that several various mechanisms may contribute to age-related accumulation of damaged mitochondria following initial oxidative injury. Such mechanisms may include clonal expansion of defective mitochondria, decreased propensity of altered mitochondria to become autophagocytosed (due to mitochondrial enlargement or decreased membrane damage associated with weakened respiration), suppressed autophagy because of heavy lipofuscin loading of lysosomes, and decreased efficiency of Lon protease. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：701 / 705

页数：5

共 36 条

[1] Mitochondrial DNA deletion mutations and sarcopenia [J].

Aiken, J ;

Bua, E ;

Cao, ZJ ;

Lopez, M ;

Wanagat, J ;

McKenzie, D ;

McKiernan, S .

INCREASING HEALTHY LIFE SPAN: CONVENTIONAL MEASURES AND SLOWING THE INNATE AGING PROCESS, 2002, 959 :412-423

[2] MITOCHONDRIAL DECAY IN AGING [J].

AMES, BN ;

SHIGENAGA, MK ;

HAGEN, TM .

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1995, 1271 (01) :165-170

[3]

[Anonymous], [No title captured]

[4] MYOCYTE CELL LOSS AND MYOCYTE CELLULAR HYPERPLASIA IN THE HYPERTROPHIED AGING RAT-HEART [J].

ANVERSA, P ;

PALACKAL, T ;

SONNENBLICK, EH ;

OLIVETTI, G ;

MEGGS, LG ;

CAPASSO, JM .

CIRCULATION RESEARCH, 1990, 67 (04) :871-885

[5] Ventricular myocytes are not terminally differentiated in the adult mammalian heart [J].

Anversa, P ;

Kajstura, J .

CIRCULATION RESEARCH, 1998, 83 (01) :1-14

[6] Changes in rat liver mitochondria with aging -: Lon protease-like activity and Nε-carboxymethyllysine accumulation in the matrix [J].

Bakala, H ;

Delaval, E ;

Hamelin, M ;

Bismuth, J ;

Borot-Laloi, C ;

Corman, B ;

Friguet, B .

EUROPEAN JOURNAL OF BIOCHEMISTRY, 2003, 270 (10) :2295-2302

[7]

BEREGI E, 1988, Z GERONTOL, V21, P83

[8] Modulation of Lon protease activity and aconitase turnover during aging and oxidative stress [J].

Bota, DA ;

Van Remmen, H ;

Davies, KJA .

FEBS LETTERS, 2002, 532 (1-2) :103-106

[9] Lipofuscin: Mechanisms of age-related accumulation and influence on cell function [J].

Brunk, UT ;

Terman, A .

FREE RADICAL BIOLOGY AND MEDICINE, 2002, 33 (05) :611-619

[10] The mitochondrial-lysosomal axis theory of aging - Accumulation of damaged mitochondria as a result of imperfect autophagocytosis [J].

Brunk, UT ;

Terman, A .

EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (08) :1996-2002

← 1 2 3 4 →