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http://www3.interscience.wiley.com – Cardiac myocytes react to diverse mechanical demands with a multitude of transient and long-term responses to normalize the cellular mechanical environment. Several stretch-activated signaling pathways have been identified, most prominently guanine nucleotide binding proteins (G-proteins), mitogen-activated protein kinases (MAPK), Janus-associated kinase/signal transducers and activators of transcription (JAK/STAT), protein kinase C (PKC), calcineurin, intracellular calcium regulation, and several autocrine and paracrine factors. Multiple levels of crosstalk exist between pathways. Read more »

http://www.sciencedirect.com – Deletion or mutation of a variety of proteins localized at cell-matrix and cell-cell junctions, such as vinculin and its splice-variant metavinculin, can lead to dilated cardiomyopathy in mice and humans, leading some to hypothesize that these molecules are involved in mechanotransmission or mechanotransduction in the heart. To investigate cardiac mechanotransduction mechanisms in single cells, we have combined laser tweezers with a fluorescence resonance energy transfer (FRET) biosensor to apply localized forces and probe localized signaling events in isolated mouse ventricular myocytes. Read more »

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http://www.sciencedirect.com – In heart muscle a mechanical stimulus is sensed and transformed into adaptive changes in cardiac function by a process called mechanotransduction. Adaptation of heart muscle to mechanical load consists of neurohumoral activation and growth, both of which decrease the initial load. Under prolonged overload this process becomes maladaptive, leading to the development of left ventricular hypertrophy and ultimately to heart failure. Read more »

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