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Roles of renin-angiotensin system and Wnt pathway in aging-related phenotypes

Takehiro Kamo1, Hiroshi Akazawa1,2, Jun-Ichi Suzuki3

  • 1Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655 Japan.

Inflammation and Regeneration
|December 21, 2017
PubMed

Insights

The renin-angiotensin system (RAS) and Wnt signaling pathway both influence aging. Blocking RAS may slow aging by down-regulating Wnt signaling, revealing a key relationship in aging processes.

Area of Science:

  • Physiology
  • Molecular Biology
  • Gerontology

Background:

  • The renin-angiotensin system (RAS) is vital for organ function but also drives aging and disease.
  • The Wnt signaling pathway is essential for survival and significantly promotes aging.
  • Both RAS and Wnt signaling exhibit antagonistic pleiotropy during growth and aging.

Purpose of the Study:

  • To review the roles of RAS and Wnt signaling in aging.
  • To explore their involvement in aging-related diseases.
  • To highlight the hierarchical relationship between RAS and Wnt signaling in aging phenotypes.

Main Methods:

  • Review of existing literature on RAS and Wnt signaling in aging.
  • Analysis of studies investigating the effects of RAS blockade on aging phenotypes.
  • Examination of the interplay between RAS and Wnt pathways in promoting aging.

Main Results:

  • RAS blockade demonstrates anti-aging effects.
  • RAS blockade is associated with the down-regulation of the canonical Wnt signaling pathway.
  • This suggests a hierarchical relationship where RAS signaling influences Wnt signaling in aging.

Conclusions:

  • RAS and Wnt signaling pathways are key regulators of the aging process.
  • Their intricate relationship, particularly the impact of RAS on Wnt, offers insights into aging mechanisms.
  • Understanding this interplay may lead to novel therapeutic strategies for age-related diseases and longevity.
Keywords:
ARBAT1 receptorCardiovascular diseaseComplement C1qSkeletal muscle regeneration

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