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Redox Stress Defines the Small Artery Vasculopathy of Hypertension: How Do We Bridge the Bench-to-Bedside Gap?
| Content Provider | Semantic Scholar |
|---|---|
| Author | Touyz, Rhian M. Montezano, Augusto Cesar Rios, Francisco J. O. Widlansky, Michael E. Liang, Mingyu |
| Copyright Year | 2017 |
| Abstract | Although 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. Considering the high prevalence of hypertension worldwide, the excess heart disease and stroke that it predisposes to, and the fact that it is the strongest modifiable risk factor for cardiovascular disease, it is not surprising that the American Heart Association funded a Strategically Focused Research Network on hypertension and that the Lancet commissioned a call-to-action and a life-course strategy to address the global burden of raised blood pressure (BP).1 Despite significant advances in understanding the pathophysiology of hypertension and the availability of numerous effective drugs, suboptimal BP control remains the primary predisposing factor for cardiovascular morbidity and mortality. This Hypertension Paradox of more uncontrolled hypertension despite improved therapies, defined by Chobanian,2 is multifactorial and may relate largely to the still unknown genetic basis and elusive causal molecular mechanisms of hypertension. Genetics plays some role in human primary hypertension as evidenced in twin studies and monogenetic forms of hypertension where the kidney is a key target. Genome-wide association studies have been disappointing and have failed to identify specific genes that underpin hypertension. Few loci have been validated or translated into therapeutic targets, with multiple genes and their variants collectively accounting for <2.5% of BP variation. In one of … |
| Starting Page | 1721 |
| Ending Page | 1723 |
| Page Count | 3 |
| File Format | PDF HTM / HTML |
| DOI | 10.1161/CIRCRESAHA.117.310672 |
| PubMed reference number | 28546356 |
| Journal | Medline |
| Volume Number | 120 |
| Issue Number | 11 |
| Alternate Webpage(s) | http://eprints.gla.ac.uk/142004/1/142004.pdf |
| Alternate Webpage(s) | https://doi.org/10.1161/CIRCRESAHA.117.310672 |
| Journal | Circulation research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
