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ATP-dependent chromatin remodeling complexes in embryonic vascular development and hypertension

*Corresponding author for this work
Research Output:
Contribution to journal
Review article
Peer-review

Abstract

Hypertension, a chronic elevation in blood pressure, is the largest single contributing factor to mortality worldwide and the most common preventable risk factor for cardiovascular disease. High blood pressure increases the risk for someone to experience a number of adverse cardiovascular events including heart failure, stroke, or aneurysm. Despite advancements in understanding factors that contribute to hypertension, the etiology remains elusive and there remains a critical need to develop innovative study approaches to develop more effective therapeutics. ATP-dependent chromatin remodelers are dynamic regulators of DNA-histone bonds and thus gene expression. The goal of this review is to highlight and summarize reports of ATP-dependent chromatin remodelers contribution to the development or maintenance of hypertension. Emerging evidence from hypertensive animal models suggests that induction of chromatin remodeler activity increases proinflammatory genes and increases blood pressure, whereas human studies demonstrate how chromatin remodelers may act as stress-response sensors to harmful physiological stimuli. Importantly, genomic studies have linked patients with hypertension to mutations in chromatin remodeler genes. Collectively, evidence linking chromatin remodelers and hypertension warrants additional research and ultimately could reveal novel therapeutic approaches for treating this complex and devastating disease.

Bibliographic Information

Output type

Research Output:
Contribution to journal
Review article
Peer-review

Original language

English

Pages from-to (Number of pages)

Pages H575-H580

Journal (Volume, Issue Number)

American Journal of Physiology - Heart and Circulatory Physiology (Volume 317, Issue 3)

Publication milestones

  • Published - 01/2019

Publication status

Published - 01/2019

ISSN

0363-6135

Publication IDs

  • Scopus: 85071711820
  • PubMed: 31398060