Mechanotransduction gone awry

By D. Jaalouk, J. Lammerding. Nature reviews. Molecular cell biology, 2009

1,364 citations recorded by the source corpus.

Cells sense their physical surroundings through mechanotransduction — that is, by translating mechanical forces and deformations into biochemical signals such as changes in intracellular calcium concentration or by activating diverse signalling pathways. In turn, these signals can adjust cellular and extracellular structure. This mechanosensitive feedback modulates cellular functions as diverse as migration, proliferation, differentiation and apoptosis, and is crucial for organ development and homeostasis. Consequently, defects in mechanotransduction — often caused by mutations or misregulation of proteins that disturb cellular or extracellular mechanics — are implicated in the development of various diseases, ranging from muscular dystrophies and cardiomyopathies to cancer progression and metastasis.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/33fe54d84fb1fef5d3f6d446bcfea2b19e47b8db

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Citations in the corpus

Review on Cell Mechanics: Experimental and Modeling Approaches (2013, neutral): “4) [43].”
Mechanotransduction at a distance: mechanically coupling the extracellular matrix with the nucleus (2009, background): “In this type of prestressed inhomogeneous solid structure, mechanical signals propagate through the cytoplasm much quicker than diffusion-based chemical signals ( Box 1 ) (see the Review by Jaalouk and Lammerdin”
Balancing forces: architectural control of mechanotransduction (2011, neutral): “Diseases such as atherosclerosis, arthritis, deafness, osteoporosis and cancer, and a number of developmental disorders, including Kartagener's syndrome and Hutchinson–Gilford progeria syndrome , commonly result from an abnormal physiological response to extrinsic (applied) or intrinsic (cell-gen”
Engineering microscale topographies to control the cell–substrate interface (2012, background): “RhoA and its effector RhoA kinase (ROCK) are known to be involved in actin remodeling and modulation of transcription factors and gene expression [20,70].”
Mechanotransduction in vascular physiology and atherogenesis (2009, background): “, and mutations in genes for cilia proteins give rise to polycystic kidney disease, possibly owing to a failure of kidney tubule cells to sense the flow of urine down the nephron (see the Review by Jaalouk and Lammerdin”
Actin dynamics, architecture, and mechanics in cell motility. (2014, background): “Another role of the cytoskeleton in disease is indirect via transmission of external forces to the nucleus, which in turn activates different pathways of gene expression and alters cell behavior (71, 90, 135, 136, 138, 321).”
Piezo1, a mechanically activated ion channel, is required for vascular development in mice (2014, background): “Biotechniques 39(5):650, 652, 654 passim.”
Role of YAP/TAZ in mechanotransduction (2011, background): “3d and Supplementary Figs 24, 25 and data not shown); (2) TAZ degradation (Fig.”
The biology of YAP/TAZ: hippo signaling and beyond. (2014, background): “Cell mechanics and the status of the cytoskeleton are true overarching signals that cells use to make essential decisions, such as proliferation, differentiation, and maintenance of stem cells (48, 95, 131, 225).”