Childhood psychosocial stress is linked with impaired vascular endothelial function, lower SIRT1, and oxidative stress in young adulthood-Reference-Cited by-同舟云学术

Childhood psychosocial stress is linked with impaired vascular endothelial function, lower SIRT1, and oxidative stress in young adulthood

Published:2021-09-01 Issue:3 Volume:321 Page:H532-H541
ISSN:0363-6135
Container-title:American Journal of Physiology-Heart and Circulatory Physiology
language:en
Short-container-title:American Journal of Physiology-Heart and Circulatory Physiology

Author:

Jenkins Nathaniel D. M.¹²^ORCID,Rogers Emily M.¹,Banks Nile F.¹,Tomko Patrick M.³^ORCID,Sciarrillo Christina M.⁴,Emerson Sam R.⁴,Taylor Ashlee⁵,Teague T. Kent⁵⁶⁷⁸

Affiliation:

1. Integrative Laboratory of Applied Physiology and Lifestyle Medicine, University of Iowa, Iowa City, Iowa

2. Abboud Cardiovascular Research Center, University of Iowa, Iowa City, Iowa

3. School of Health Sciences, Kent State University, Kent, Ohio

4. Laboratory of Applied Nutrition and Exercise Science, Oklahoma State University, Tulsa, Oklahoma

5. Integrative Immunology Center, University of Oklahoma School of Community Medicine, Tulsa, Oklahoma

6. Department of Surgery, University of Oklahoma School of Community Medicine, Tulsa, Oklahoma

7. Department of Psychiatry, University of Oklahoma School of Community Medicine, Tulsa, Oklahoma

8. Department of Biochemistry and Microbiology, Oklahoma State University Center for Health Sciences, Tulsa, Oklahoma

Abstract

Our study provides novel evidence that young adult women with moderate-to-severe adverse childhood experience (ACE) exposure present impaired endothelial function and lower circulating sirtuin 1 (SIRT1) concentrations than age-matched controls. However, an 8-wk exercise intervention was unable to augment endothelial function or SIRT1 concentrations in a subset of those with ACEs. Our data suggest that ACEs-related impairments in endothelial function may be secondary to decreased NO bioavailability via SIRT1 and/or oxidative stress-related mechanisms.

Funder

HHS | NIH | National Institute of General Medical Sciences

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpheart.00123.2021

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