4.7 Article

Integrin signaling: linking mechanical stimulation to skeletal muscle hypertrophy

Journal

AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 317, Issue 4, Pages C629-C641

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00009.2019

Keywords

hypertrophy; ILK; integrin; mTORC; skeletal muscle

Funding

  1. National Institute of Arthritis and Musculoskeletal and Skin Diseases [R21-AR-065578]

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The alpha(7)beta(1)-integrin is a transmembrane adhesion protein that connects laminin in the extracellular matrix (ECM) with actin in skeletal muscle fibers. The alpha(7)beta(1)-integrin is highly expressed in skeletal muscle and is concentrated at costameres and myotendious junctions, providing the opportunity to transmit longitudinal and lateral forces across the membrane. Studies have demonstrated that alpha(7) -integrin subunit mRNA and protein are upregulated following eccentric contractions as a mechanism to reinforce load-bearing structures and resist injury with repeated bouts of exercise. It has been hypothesized for many years that the integrin can also promote protein turnover in a manner that can promote beneficial adaptations with resistance exercise training, including hypertrophy. This review provides basic information about integrin structure and activation and then explores its potential to serve as a critical mechanosensor and activator of muscle protein synthesis and growth. Overall, the hypothesis is proposed that the alpha(7)beta(1)-integrin can contribute to mechanical-load induced skeletal muscle growth via an mammalian target of rapamycin complex 1-independent mechanism.

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