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A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics
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Published on: September 19, 2016

Arginase and vascular aging.

Lakshmi Santhanam1, David W Christianson, Daniel Nyhan

  • 1Department of Biomedical Engineering, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|August 23, 2008
PubMed
Summary
This summary is machine-generated.

Arginase activation contributes to age-related vascular stiffness by limiting nitric oxide (NO) production and increasing oxidative stress. Targeting arginase may help reduce cardiovascular disease risk in aging populations.

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Published on: August 6, 2020

Area of Science:

  • Cardiovascular Physiology
  • Aging Research
  • Endothelial Function

Background:

  • Vascular and ventricular stiffness are key features of cardiovascular aging.
  • Endothelial dysfunction, marked by increased reactive oxygen species (ROS) and decreased nitric oxide (NO) bioavailability, drives vascular stiffness.
  • Arginase activation is implicated in age-related endothelial dysfunction.

Purpose of the Study:

  • To investigate the role of arginase in age-related vascular stiffness and endothelial dysfunction.
  • To explore the mechanisms by which arginase contributes to vascular aging, including NO signaling and other pathways.

Main Methods:

  • Analysis of arginase activation and its impact on NO synthase (NOS) activity in aging vascular models.
  • Investigation of posttranslational modifications, such as S-nitrosylation, affecting arginase activity.
  • Assessment of arginase-dependent mechanisms beyond NO signaling, including polyamine-mediated effects on vascular smooth muscle cells and collagen synthesis.

Main Results:

  • Arginase activation limits L-arginine availability for NOS3, reducing NO synthesis and enhancing ROS production by NOS.
  • Increased arginase abundance and S-nitrosylation (mediated by NOS2 induction) contribute to enhanced enzyme activity in aging vasculature.
  • Arginase activation promotes vascular aging through non-NO-dependent pathways, such as polyamine-driven smooth muscle proliferation and collagen synthesis.

Conclusions:

  • Arginase plays a significant role in age-related endothelial dysfunction and vascular stiffness.
  • Arginase contributes to vascular aging via both NO-dependent and NO-independent mechanisms.
  • Arginase represents a potential therapeutic target for mitigating age-related cardiovascular stiffness and associated morbidity/mortality.