ライブラリ登録: Guest
Begell Digital Portal Begellデジタルライブラリー 電子書籍 ジャーナル 参考文献と会報 リサーチ集
Critical Reviews™ in Eukaryotic Gene Expression
インパクトファクター: 1.841 5年インパクトファクター: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN 印刷: 1045-4403
ISSN オンライン: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v19.i4.50
pages 319-338

Mechanical Signaling for Bone Modeling and Remodeling

Alexander G. Robling
Department of Anatomy & Cell Biology, Indiana University School of Medicine; Department of Biomedical Engineering, Indiana University/Purdue University at Indianapolis (IUPUI)
Charles H. Turner
Indiana University

要約

Proper development of the skeleton in utero and during growth requires mechanical stimulation. Loading results in adaptive changes in bone that strengthen bone structure. Bone’s adaptive response is regulated by the ability of resident bone cells to perceive and translate mechanical energy into a cascade of structural and biochemical changes within the cells — a process known as mechanotransduction. Mechanotransduction pathways are among the most anabolic in bone, and consequently, there is great interest in elucidating how mechanical loading produces its observed effects, including increased bone formation, reduced bone loss, changes in bone cell differentiation and lifespan, among others. A molecular understanding of these processes is developing, and with it comes a profound new insight into the biology of bone. In this article, we review the nature of the physical stimulus to which bone cells mount an adaptive response, including the identity of the sensor cells, their attributes and physical environment, and putative mechanoreceptors they express. Particular attention is allotted to the focal adhesion and Wnt signaling, in light of their emerging role in bone mechanotransduction. Te cellular mechanisms for increased bone loss during disuse, and reduced bone loss during loading are considered. Finally, we summarize the published data on bone cell accommodation, whereby bone cells stop responding to mechanical signaling events. Collectively, these data highlight the complex yet finely orchestrated process of mechanically regulated bone homeostasis.


Articles with similar content:

The Cellular and Clinical Parameters of Anabolic Therapy for Osteoporosis
Critical Reviews™ in Eukaryotic Gene Expression, Vol.13, 2003, issue 1
Clifford J. Rosen
Molecular Mechanisms in Coupling of Bone Formation to Resorption
Critical Reviews™ in Eukaryotic Gene Expression, Vol.19, 2009, issue 1
T. John Martin, Jonathan H. Gooi, Natalie A. Sims
Muller Glia in Retinal Innate Immunity: A Perspective on Their Roles in Endophthalmitis
Critical Reviews™ in Immunology, Vol.33, 2013, issue 2
Mamta Kanwar, Lindsay J. Miller, Ashok Kumar, Pawan K. Singh, Rajeev K. Pandey
Signaling Networks that Control the Lineage Commitment and Differentiation of Bone Cells
Critical Reviews™ in Eukaryotic Gene Expression, Vol.19, 2009, issue 1
Shuying Yang, Wei Chen, Carrie S. Soltanoff, Yi-Ping Li
Monogenic and Complex Forms of Obesity: Insights from Genetics Reveal the Leptin-Melanocortin Signaling Pathway as a Common Player
Critical Reviews™ in Eukaryotic Gene Expression, Vol.22, 2012, issue 4
Sigri Beckers, Doreen Zegers, Luc F. Van Gaal, Wim Van Hul