Chen Songcang, Agrawal Devendra K
Department of Biomedical Sciences and Center for Clinical & Translational Science, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE, 68178, USA,
Curr Hypertens Rep. 2015 Feb;17(2):8. doi: 10.1007/s11906-014-0521-1.
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.
原发性高血压（EH）及其并发症对公众健康造成了严重影响。然而，EH发病机制的潜在机制在很大程度上仍不清楚。最近主要在大鼠和小鼠身上进行的研究提供了证据，表明T淋巴细胞亚群不同功能的失调是高血压发病机制中一个潜在的重要机制。我们批判性地回顾了最近的研究结果，并对高血压发病机制中功能失调的T淋巴细胞亚群的理解提出了另一种解释。假说是高血压刺激直接或间接增加心血管系统和肾脏中的局部白细胞介素-6水平，这可能会促进外周Th17细胞和调节性T细胞分化及比例失衡。这导致血管周围脂肪组织和外膜中白细胞介素-17增加而白细胞介素-10减少，从而促成实验动物模型中高血压的发展。该领域需要进一步研究，以推动新的转化进展，从而促进对EH发病机制的理解，并开发预防和治疗EH的新方法。
