Why the study?
Understanding of how mechanical signals are sensed and transduced by cardiomyocytes is limited despite the recognized importance of mechanical signaling in cardiac cells.
This review highlights emerging in vitro platforms that better recapitulate pathological extracellular matrix stiffness changes to advance the understanding of cardiomyocyte mechanobiology.
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May inform in vitro model development for mechanobiology research; leaves open clinical translation of ECM remodeling insights.
Mechanobiology-a cell's interaction with its physical environment-can influence a myriad of cellular processes including how cells migrate, differentiate and proliferate. In many diseases, remodeling of the extracellular matrix (ECM) is observed such as tissue stiffening in rigid scar formation after myocardial infarct. Utilizing knowledge of cell mechanobiology in relation to ECM remodeling during pathogenesis, elucidating the role of the ECM in the progression-and perhaps regression-of disease is a primary focus of the field. Although the importance of mechanical signaling in the cardiac cell is well-appreciated, our understanding of how these signals are sensed and transduced by cardiomyocytes is limited. To overcome this limitation, recently developed tools and resources have provided exciting opportunities to further our understandings by better recapitulating pathological spatiotemporal ECM stiffness changes in an in vitro setting. In this review, we provide an overview of a conventional model of mechanotransduction and present understandings of cardiomyocyte mechanobiology, followed by a review of emerging tools and resources that can be used to expand our knowledge of cardiomyocyte mechanobiology toward more clinically relevant applications.
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Chin et al. (2019) studied this question.
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