Renin-angiotensin system: An old player with novel functions in skeletal muscle

Claudio Cabello-Verrugio*, María Gabriela Morales, Juan Carlos Rivera, Daniel Cabrera, Felipe Simon

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

120 Scopus citations

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.

Original languageEnglish
Pages (from-to)437-463
Number of pages27
JournalMedicinal Research Reviews
Volume35
Issue number3
DOIs
StatePublished - 1 May 2015
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2015 Wiley Periodicals, Inc.

Keywords

  • Angiotensin (1-7)
  • Angiotensin II
  • Atrophy
  • Fibrosis
  • Insulin resistance
  • Skeletal muscle

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