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Mechanotransduction in Cardiac Myocytes
JAN LAMMERDINGa,
ROGER D. KAMMa AND
RICHARD T. LEEa,b
aBiological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
bCardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA
Address for correspondence: Prof. Richard T. Lee, M.D., Brigham & Women's Hospital, Harvard Medical School, 65 Landsdowne Street, Cambridge, MA 02139. Fax: 617-768-8270. rlee{at}rics.bwh.harvard.edu
Ann. N.Y. Acad. Sci. 1015: 53-70 (2004).
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. The cellular response to changes in the mechanical environment can lead to cardiac myocyte hypertrophy, cellular growth that can be accompanied by pathological myocyte dysfunction, and tissue fibrosis. Several candidates for the primary mechanosensor in cardiac myocytes have been identified, ranging from stretch-activated ion channels in the membrane to yet-unknown mechanosensitive mechanisms in the nucleus. New and refined experimental techniques will exploit advances in molecular biology and biological imaging to study mechanotransduction in isolated cells and genetically engineered mice to explore the function of individual proteins.
Key Words: mechanotransduction • cardiac hypertrophy • cardiac myocytes
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