Cardiovascular Program, Monash Biomedicine Discovery Institute, Monash University, Melbourne, Australia
Department of Physiology, Monash University, Melbourne, Australia.
Clin Sci (Lond). 2018 Jan 2;132(1):33-36. doi: 10.1042/CS20171366. Print 2018 Jan 16.
In a recent issue of Clinical Science, Stanhewicz et al. investigated persistent microvascular dysfunction in women up to 16 months postpartum. The authors found sensitivity to the pressor effects of endothelin-1 (ET-1) was enhanced when compared with women who had a normotensive pregnancy. Importantly, the authors demonstrated that this effect was mediated via the endothelin type B (ET) receptors. Therefore, the present study highlights the possibility that alterations in the localization of the ET receptor contributes to the pathogenesis of pre-eclampsia and future cardiovascular disease (CVD) risk. Currently, there is great interest in the role of the endothelin system in pre-eclampsia. Targetting the endothelin system, potentially by modulating upstream pathways to prevent ET receptor dysfunction, may improve health outcomes for women and their offspring during pre-eclampsia and later life.
在最近一期的《临床科学》杂志上,Stanhewicz 等人研究了多达 16 个月产后女性持续存在的微血管功能障碍。与血压正常妊娠的女性相比,作者发现其对内皮素-1(ET-1)升压作用的敏感性增强。重要的是,作者证明这种作用是通过内皮素 B 型(ETB)受体介导的。因此,本研究强调了 ET 受体定位改变可能导致子痫前期和未来心血管疾病(CVD)风险的可能性。目前,内皮素系统在子痫前期中的作用引起了广泛关注。靶向内皮素系统,可能通过调节上游途径来防止 ET 受体功能障碍,可能会改善子痫前期和以后生活中女性及其后代的健康结局。