title: Renin-angiotensin system: an old player with novel functions in skeletal muscle.
abstract: Skeletal muscle is a tissue that shows the most plasticity in the body; it can change in response to physiological and pathological stimuli. Among the diseases that affect skeletal muscle are myopathy-associated fibrosis, insulin resistance, and muscle atrophy. A common factor in these pathologies is the participation of the renin-angiotensin system (RAS). This system can be functionally separated into the classical and nonclassical RAS axis. The main components of the classical RAS pathway are angiotensin-converting enzyme (ACE), angiotensin II (Ang-II), and Ang-II receptors (AT receptors), whereas the nonclassical axis is composed of ACE2, angiotensin 1-7 [Ang (1-7)], and the Mas receptor. Hyperactivity of the classical axis in skeletal muscle has been associated with insulin resistance, atrophy, and fibrosis. In contrast, current evidence supports the action of the nonclassical RAS as a counter-regulator axis of the classical RAS pathway in skeletal muscle. In this review, we describe the mechanisms involved in the pathological effects of the classical RAS, advances in the use of pharmacological molecules to inhibit this axis, and the beneficial effects of stimulation of the nonclassical RAS pathway on insulin resistance, atrophy, and fibrosis in skeletal muscle.
authors.affiliation: Laboratorio de Biología y Fisiopatología Molecular, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas & Facultad de Medicina, Universidad Andres Bello, Santiago, Chile.
authors.forename: Claudio
authors.initials: C
authors.lastname: Cabello-Verrugio
authors.forename: María Gabriela
authors.initials: MG
authors.lastname: Morales
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Rivera
authors.forename: Daniel
authors.initials: D
authors.lastname: Cabrera
authors.forename: Felipe
authors.initials: F
authors.lastname: Simon
mesh_terms: D000818:Animals; D001284:Atrophy; D005355:Fibrosis; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D051379:Mice; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D007703:Peptidyl-Dipeptidase A / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology*
chemical_list: C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A; D005947:Glucose
keywords: angiotensin (1-7); angiotensin II; atrophy; fibrosis; insulin resistance; skeletal muscle