cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism and regeneratio

[Mike Bikov]

Am J Physiol Endocrinol Metab. 2012 Feb 21. [Epub ahead of print]
cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism and regeneration.
Berdeaux R, Stewart R.
Source

1University of Texas Health Science Center at Houston.
Abstract

Among organ systems, skeletal muscle is perhaps the most structurally specialized. The remarkable subcellular architecture of this tissue allows it to empower movement with instruction from motor neurons. Despite this high degree of specialization, skeletal muscle also has intrinsic signaling mechanisms that allow adaptation to long-term changes in demand and regeneration after acute damage. The second messenger 3'-5'-cyclic adenosine monophosphate (cAMP) not only elicits acute changes within myofibers during exercise but also contributes to myofiber size and metabolic phenotype in the long term. Strikingly, sustained activation of cAMP signaling leads to pronounced hypertrophic responses in skeletal myofibers through largely elusive molecular mechanisms. These pathways can promote hypertrophy and combat atrophy in animal models of disorders including muscular dystrophy, age-related atrophy, denervation injury, disuse atrophy, cancer cachexia and sepsis. cAMP also participates in muscle development and regeneration mediated by muscle precursor cells, and thus downstream signaling pathways may potentially be harnessed to promote muscle regeneration in patients with acute damage or muscular dystrophy. In this review we will summarize studies implicating cAMP signaling in skeletal muscle adaptation. We will also highlight ligands that induce cAMP signaling and downstream effectors that are promising pharmacologic targets.​

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