Abstract
Essential hypertension (EH) and its complications have had a severe impact on public health. However, the underlying mechanisms of the pathogenesis of EH remain largely unknown. Recent investigations, predominantly in rats and mice, have provided evidence that dysregulation of distinct functions of T lymphocyte subsets is a potentially important mechanism in the pathogenesis of hypertension. We critically reviewed recent findings and propose an alternative explanation on the understanding of dysfunctional T lymphocyte subsets in the pathogenesis of hypertension. The hypothesis is that hypertensive stimuli, directly and indirectly, increase local IL-6 levels in the cardiovascular system and kidney, which may promote peripheral imbalance in the differentiation and ratio of Th17 and T regulatory cells. This results in increased IL-17 and decreased IL-10 in perivascular adipose tissue and adventitia contributing to the development of hypertension in experimental animal models. Further investigation in the field is warranted to inform new translational advances that will promote to understand the pathogenesis of EH and develop novel approaches to prevent and treat EH.
| Original language | English |
|---|---|
| Journal | Current Hypertension Reports |
| Volume | 17 |
| Issue number | 2 |
| DOIs | |
| State | Published - Feb 1 2015 |
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All Science Journal Classification (ASJC) codes
- Internal Medicine
- Medicine(all)
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Dysregulation of T cell Subsets in the Pathogenesis of Hypertension. / Chen, Songcang; Agrawal, Devendra K.
In: Current Hypertension Reports, Vol. 17, No. 2, 01.02.2015.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Dysregulation of T cell Subsets in the Pathogenesis of Hypertension
AU - Chen, Songcang
AU - Agrawal, Devendra K.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - Essential hypertension (EH) and its complications have had a severe impact on public health. However, the underlying mechanisms of the pathogenesis of EH remain largely unknown. Recent investigations, predominantly in rats and mice, have provided evidence that dysregulation of distinct functions of T lymphocyte subsets is a potentially important mechanism in the pathogenesis of hypertension. We critically reviewed recent findings and propose an alternative explanation on the understanding of dysfunctional T lymphocyte subsets in the pathogenesis of hypertension. The hypothesis is that hypertensive stimuli, directly and indirectly, increase local IL-6 levels in the cardiovascular system and kidney, which may promote peripheral imbalance in the differentiation and ratio of Th17 and T regulatory cells. This results in increased IL-17 and decreased IL-10 in perivascular adipose tissue and adventitia contributing to the development of hypertension in experimental animal models. Further investigation in the field is warranted to inform new translational advances that will promote to understand the pathogenesis of EH and develop novel approaches to prevent and treat EH.
AB - Essential hypertension (EH) and its complications have had a severe impact on public health. However, the underlying mechanisms of the pathogenesis of EH remain largely unknown. Recent investigations, predominantly in rats and mice, have provided evidence that dysregulation of distinct functions of T lymphocyte subsets is a potentially important mechanism in the pathogenesis of hypertension. We critically reviewed recent findings and propose an alternative explanation on the understanding of dysfunctional T lymphocyte subsets in the pathogenesis of hypertension. The hypothesis is that hypertensive stimuli, directly and indirectly, increase local IL-6 levels in the cardiovascular system and kidney, which may promote peripheral imbalance in the differentiation and ratio of Th17 and T regulatory cells. This results in increased IL-17 and decreased IL-10 in perivascular adipose tissue and adventitia contributing to the development of hypertension in experimental animal models. Further investigation in the field is warranted to inform new translational advances that will promote to understand the pathogenesis of EH and develop novel approaches to prevent and treat EH.
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UR - http://www.scopus.com/inward/citedby.url?scp=84926390431&partnerID=8YFLogxK
U2 - 10.1007/s11906-014-0521-1
DO - 10.1007/s11906-014-0521-1
M3 - Review article
VL - 17
JO - Current Hypertension Reports
JF - Current Hypertension Reports
SN - 1522-6417
IS - 2
ER -