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Journal ArticleDOI

An introductory review of cell mechanobiology.

TLDR
Future research in the area of cell mechanobiology will require novel experimental and theoretical methodologies to determine the type and magnitude of the forces experienced at the cellular and sub-cellular levels and to identify the force sensors/receptors that initiate the cascade of cellular and molecular events.
Abstract
Mechanical loads induce changes in the structure, composition, and function of living tissues. Cells in tissues are responsible for these changes, which cause physiological or pathological alterations in the extracellular matrix (ECM). This article provides an introductory review of the mechanobiology of load-sensitive cells in vivo, which include fibroblasts, chondrocytes, osteoblasts, endothelial cells, and smooth muscle cells. Many studies have shown that mechanical loads affect diverse cellular functions, such as cell proliferation, ECM gene and protein expression, and the production of soluble factors. Major cellular components involved in the mechanotransduction mechanisms include the cytoskeleton, integrins, G proteins, receptor tyrosine kinases, mitogen-activated protein kinases, and stretch-activated ion channels. Future research in the area of cell mechanobiology will require novel experimental and theoretical methodologies to determine the type and magnitude of the forces experienced at the cellular and sub-cellular levels and to identify the force sensors/receptors that initiate the cascade of cellular and molecular events

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Citations
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Journal ArticleDOI

Mechanotransduction and extracellular matrix homeostasis

TL;DR: Progress towards understanding the molecular, cellular and tissue-level effects that promote mechanical homeostasis has helped to identify key questions for future research.
Journal ArticleDOI

The small GTP-binding protein rho regulates the assembly of focal adhesions and actin stress fibers in response to growth factors

TL;DR: In this paper, rho, a ras-related GTP-binding protein, rapidly stimulated stress fiber and focal adhesion formation when microinjected into serum-starved Swiss 3T3 cells.
Journal ArticleDOI

Microengineered Platforms for Cell Mechanobiology

TL;DR: In this article, the authors discuss emerging bioengineered tools enabled by micro-scale technologies for studying the roles of mechanical forces in cell biology and discuss how microengineered platforms can be used to generate in vivo-like micromechanical environment in in vitro settings for investigating cellular processes in normal and pathophysiological contexts.
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Integrins in mechanotransduction

TL;DR: Effects of forces on organs, tissues, and cells are summarized; recent advances toward understanding molecular mechanisms are discussed; and the role of Integrin-mediated adhesions is discussed.
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Elastic theory of unconstrained non-Euclidean plates

TL;DR: In this paper, the authors present a mathematical framework for non-Euclidean plates in terms of a covariant theory of linear elasticity, valid for large displacements.
References
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Journal ArticleDOI

The pathogenesis of atherosclerosis: a perspective for the 1990s

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Signal transduction by receptors with tyrosine kinase activity

TL;DR: Cet article synthese montre comment des recepteurs membranaires a activite tyrosine kinase peuvent etre impliques dans la transduction and notamment jouent le role de signal de the transduction.
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The Pathogenesis of Atherosclerosis — An Update

TL;DR: A response-to-injury hypothesis of atherogenesis proposes that "injury" to the endothelium is the initiating event in atherosclerosis, and intimal smooth-muscle proliferation as the key event in the development of the advanced lesions of Atherosclerosis.
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Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry.

TL;DR: This review describes the members of the matrixin family and discusses substrate specificity, domain structure and function, the activation of proMMPs, the regulation of matrixin activity by tissue inhibitors of metalloproteinases, and their pathophysiological implication.
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