A2 Vertaisarvioitu katsausartikkeli tieteellisessä lehdessä

Notch in mechanotransduction - from molecular mechanosensitivity to tissue mechanostasis




TekijätStassen Oscar MJA, Ristori Tommaso, Sahlgren Cecilia M

KustantajaCompany of Biologists Ltd

Julkaisuvuosi2020

JournalJournal of Cell Science

Tietokannassa oleva lehden nimiJournal of cell science

Lehden akronyymiJ Cell Sci

Artikkelin numerojcs250738

Vuosikerta133

Numero24

Sivujen määrä14

ISSN0021-9533

eISSN1477-9137

DOIhttps://doi.org/10.1242/jcs.250738

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/Publication/52215637


Tiivistelmä
Tissue development and homeostasis are controlled by mechanical cues. Perturbation of the mechanical equilibrium triggers restoration of mechanostasis through changes in cell behavior, while defects in these restorative mechanisms lead to mechanopathologies, for example, osteoporosis, myopathies, fibrosis or cardiovascular disease. Therefore, sensing mechanical cues and integrating them with the biomolecular cell fate machinery is essential for the maintenance of health. The Notch signaling pathway regulates cell and tissue fate in nearly all tissues. Notch activation is directly and indirectly mechanosensitive, and regulation of Notch signaling, and consequently cell fate, is integral to the cellular response to mechanical cues. Fully understanding the dynamic relationship between molecular signaling, tissue mechanics and tissue remodeling is challenging. To address this challenge, engineered microtissues and computational models play an increasingly large role. In this Review, we propose that Notch takes on the role of a 'mechanostat', maintaining the mechanical equilibrium of tissues. We discuss the reciprocal role of Notch in the regulation of tissue mechanics, with an emphasis on cardiovascular tissues, and the potential of computational and engineering approaches to unravel the complex dynamic relationship between mechanics and signaling in the maintenance of cell and tissue mechanostasis.

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