Redox Stress Defines the Small Artery Vasculopathy of Hypertension: How Do We Bridge the Bench-to-Bedside Gap? Circ Res 2017 May 26;120(11):1721-1723
Date
05/27/2017Pubmed ID
28546356Pubmed Central ID
PMC5520661DOI
10.1161/CIRCRESAHA.117.310672Scopus ID
2-s2.0-85019773728 (requires institutional sign-in at Scopus site) 14 CitationsAbstract
While convincing experimental evidence demonstrates the importance of vascular reactive oxygen and nitrogen species (RONS), oxidative stress and perturbed redox signaling as causative processes in the vasculopathy of hypertension, this has not translated to the clinic. We discuss this bench-to-bedside disparity and the urgency to progress vascular redox pathobiology from experimental models to patients by studying disease-relevant human tissues. It is only through such approaches that the unambiguous role of vascular redox stress will be defined so that mechanism-based therapies in a personalized and precise manner can be developed to prevent, slow or reverse progression of small vessel disorders and consequent hypertension.
Author List
Touyz RM, Montezano AC, Rios F, Widlansky ME, Liang MAuthor
Michael E. Widlansky MD Associate Director, Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBiomedical Research
Blood Pressure
Cerebral Small Vessel Diseases
Humans
Hypertension
Microvessels
Oxidation-Reduction
Oxidative Stress
