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Signalling protein protects the heart muscle from pressure-related stress

If blood flow from the heart is impeded, the pressure created causes tissue dysfunction. It emerges that different signals converge on the TSC2 and mTOR proteins to fine-tune the response of heart cells to stress.
  1. Brendan D. Manning

    1. Brendan D. Manning is in the Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, Massachusetts 02115, USA.

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Chronic tissue stress causes the emission of molecular signals that propagate through cellular lines of communication known as signal-transduction pathways. These pathways trigger responses that can either exacerbate tissue damage or alleviate the harmful effects of the stress. Conditions that hinder the outflow of blood from the heart, such as high blood pressure (hypertension), can induce a type of chronic stress known as pressure overload. This can, in turn, cause abnormal overgrowth of the heart muscle (cardiac hypertrophy), which can precede heart failure (Fig. 1a). Writing in Nature, Ranek et al.1 report that, in heart muscle cells (cardiomyocytes) of mice, pressure overload activates two signal-transduction pathways, one involving an enzyme complex known as mTORC1, and the other involving the enzyme PKG1. The authors show that the two pathways converge to influence the adverse consequences of this stress.

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Nature 566, 187-188 (2019)

doi: https://doi.org/10.1038/d41586-019-00245-3

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