Journal
NATURE REVIEWS MOLECULAR CELL BIOLOGY
Volume 14, Issue 1, Pages 38-48Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrm3495
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Funding
- US National Institutes of Health
- Howard Hughes Medical Institute
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R00HL112852] Funding Source: NIH RePORTER
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The heart hypertrophies in response to developmental signals as well as increased workload. Although adult-onset hypertrophy can ultimately lead to disease, cardiac hypertrophy is not necessarily maladaptive and can even be beneficial. Progress has been made in our understanding of the structural and molecular characteristics of physiological cardiac hypertrophy, as well as of the endocrine effectors and associated signalling pathways that regulate it. Physiological hypertrophy is initiated by finite signals, which include growth hormones (such as thyroid hormone, insulin, insulin-like growth factor 1 and vascular endothelial growth factor) and mechanical forces that converge on a limited number of intracellular signalling pathways (such as PI3K, AKT, AMP-activated protein kinase and mTOR) to affect gene transcription, protein translation and metabolism. Harnessing adaptive signalling mediators to reinvigorate the diseased heart could have important medical ramifications.
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