Aging bone and cartilage: cross-cutting issues

被引：60

作者：

Carrington, JL ^{[1
]}

机构：

[1] NIA, Dept Hlth & Human Serv, Biol Aging Program, NIH, Bethesda, MD 20892 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2005年 / 328卷 / 03期

关键词：

aging; cartilage; bone; osteoarthritis; osteoporosis; osteopenia; apoptosis; stem cells;

D O I：

10.1016/j.bbrc.2004.12.041

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Aging is a major risk factor for osteoarthritis and osteoporosis. Yet, these are not necessary outcomes of aging, and the relationship between age-related changes in bone and cartilage and development of disease is not clear. There are some well-described cellular changes associated with aging in multiple tissues that appear to be fundamental to the decline in function of cartilage and bone. A better understanding of age-related changes in cells and tissues is necessary to mitigate or, hopefully, avoid loss of bone and cartilage with aging. In addition, a better understanding of the dynamics of tissue maintenance in vivo is critical to developing tissue replacement and repair therapies. The role of stem cells in this process, and why tissues are not well maintained with advancing age, are frontiers for future aging research. Published by Elsevier Inc.

引用

页码：700 / 708

页数：9

共 93 条

[21] Cartilage injury induces chondrocyte apoptosis [J].

D'Lima, DD ;

Hashimoto, S ;

Chen, PC ;

Lotz, MK ;

Colwell, CW .

JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME, 2001, 83A :19-21

[22] Human chondrocyte apoptosis in response to mechanical injury [J].

D'Lima, DD ;

Hashimoto, S ;

Chen, PC ;

Colwell, CW ;

Lotz, MK .

OSTEOARTHRITIS AND CARTILAGE, 2001, 9 (08) :712-719

[23] Premature aging in mice deficient in DNA repair and transcription [J].

de Boer, J ;

Andressoo, JO ;

de Wit, J ;

Huijmans, J ;

Beems, RB ;

van Steeg, H ;

Weeda, G ;

van der Horst, GTJ ;

van Leeuwen, W ;

Themmen, APN ;

Meradji, M ;

Hoeijmakers, JHJ .

SCIENCE, 2002, 296 (5571) :1276-1279

[24] Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis [J].

DeGroot, J ;

Verzijl, N ;

Wenting-van Wijk, MJG ;

Jacobs, KMG ;

Van El, B ;

Van Roermund, PM ;

Bank, RA ;

Bijlsma, JWJ ;

TeKoppele, JM ;

Lafeber, FPJG .

ARTHRITIS AND RHEUMATISM, 2004, 50 (04) :1207-1215

[25] Accumulation of advanced glycation endproducts reduces chondrocyte-mediated extracellular matrix turnover in human articular cartilage [J].

DeGroot, J ;

Verzijl, N ;

Jacobs, KMG ;

Budde, M ;

Bank, RA ;

Bijlsma, JWJ ;

TeKoppele, JM ;

Lafeber, FPJG .

OSTEOARTHRITIS AND CARTILAGE, 2001, 9 (08) :720-726

[26] Lipid peroxidation and advanced glycation end products in the brain in normal aging and in Alzheimer's disease [J].

Dei, R ;

Takeda, A ;

Niwa, H ;

Li, M ;

Nakagomi, Y ;

Watanabe, M ;

Inagaki, T ;

Washimi, Y ;

Yasuda, Y ;

Horie, K ;

Miyata, T ;

Sobue, G .

ACTA NEUROPATHOLOGICA, 2002, 104 (02) :113-122

[27] Increased oxidative stress with aging reduces chondrocyte survival correlation with intracellular glutathione levels [J].

Del Carlo, M ;

Loeser, RF .

ARTHRITIS AND RHEUMATISM, 2003, 48 (12) :3419-3430

[28] The age of cancer [J].

DePinho, RA .

NATURE, 2000, 408 (6809) :248-254

[29] A BIOMARKER THAT IDENTIFIES SENESCENT HUMAN-CELLS IN CULTURE AND IN AGING SKIN IN-VIVO [J].

DIMRI, GP ;

LEE, XH ;

BASILE, G ;

ACOSTA, M ;

SCOTT, C ;

ROSKELLEY, C ;

MEDRANO, EE ;

LINSKENS, M ;

RUBELJ, I ;

PEREIRASMITH, O ;

PEACOCKE, M ;

CAMPISI, J .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (20) :9363-9367

[30] Insights into aging obtained from p53 mutant mouse models [J].

Dumble, M ;

Gatza, C ;

Tyner, S ;

Venkatachalam, S ;

Donehower, LA .

STRATEGIES FOR ENGINEERED NEGLIGIBLE SENESCENCE: WHY GENUINE CONTROL OF AGING MAY BE FORESEEABLE, 2004, 1019 :171-177

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