脂肪血管减少了大量的程序性心血管风险

D. Giussani
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引用次数: 0

摘要

心血管疾病仍然是当今世界上最大的杀手之一,在英国造成超过四分之一的死亡(https://www.bhf.org.uk/for-professionals/新闻中心/事实与数据)。众所周知,患心血管疾病的风险是由我们的基因构成和生活方式风险因素(如吸烟、肥胖和缺乏锻炼)之间的相互作用决定的。越来越多的人意识到,在出生前,基因与环境的相互作用,通过一个被称为发育编程的过程,在设定心血管疾病的风险方面,可能同样重要,如果不是更重要的话(Giussani & Davidge, 2013)。在人类中,支持发育规划的最佳证据来自对减肥手术前后怀孕的肥胖妇女的研究(gusamadard et al. 2013)。这些研究表明,手术前出生的兄弟姐妹比手术后出生的兄弟姐妹患心血管疾病的风险更高。因此,这些研究强调,即使在同一个子宫内,环境的变化也可能导致同一家庭后代患心血管疾病的风险差异。这为人类提供了强有力的证据,证明在发育的关键早期阶段所经历的环境质量直接影响到长期的心血管健康。毫不奇怪,这些概念更新并扩大了对预防而不是治疗的关注,以减轻心血管疾病的负担,并使预防医学在发展轨迹中尽早开始,而不是等到疾病变得不可逆转后才进行治疗。在这一期的《生理学杂志》上,Badran等人(2019)利用已建立的小鼠模型,研究了怀孕期间阻塞性睡眠呼吸暂停对成年后代心脏代谢功能的影响。阻塞性睡眠呼吸暂停的特点是间歇性缺氧发作,这会促进氧化和炎症应激,并增加患者心血管功能障碍的风险(Badran et al. 2019)。然而,动物模型并没有解决怀孕期间母亲阻塞性睡眠呼吸暂停对胎儿的影响
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fatty vessels shed tonnes on programmed cardiovascular risk
Cardiovascular disease remains one of the greatest killers in the world today, causing more than a quarter of all deaths in the UK (https://www.bhf.org.uk/for-professionals/ press-centre/facts-and-figures). It is common knowledge that cardiovascular risk is determined by the interaction between our genetic make-up and lifestyle risk factors, such as smoking, obesity and lack of exercise. There is increasing awareness that the gene–environment interaction before birth may be just as, if not more, important in setting a risk of cardiovascular disease, through a process known as developmental programming (Giussani & Davidge, 2013). In humans, the best evidence to support developmental programming comes from studies of obese women who have fallen pregnant before and after having bariatric surgery (Guénard et al. 2013). These studies show that siblings born before the surgery have an increased risk of cardiovascular disease compared to those born after. Therefore, such studies highlight that changes in the environment even within the same womb can programme a differential risk of cardiovascular disease in offspring of the same family. This provides strong evidence in humans that the quality of the environment experienced during critical, early periods of development directly influences long-term cardiovascular health. Unsurprisingly, these concepts have renewed and amplified a focus on prevention rather than treatment to reduce the burden of cardiovascular disease, and for preventative medicine to start as early as possible in the developmental trajectory rather than waiting to treat disease after it has become irreversible. In this issue of The Journal of Physiology, Badran et al. (2019) investigated the effects of obstructive sleep apnoea during pregnancy on cardiometabolic function in the adult offspring using an established mouse model. Obstructive sleep apnoea is characterized by episodes of intermittent hypoxia, which promote oxidative and inflammatory stress, and increase the risk of cardiovascular dysfunction in affected patients (Badran et al. 2019). However, animal models have not addressed the effects of maternal obstructive sleep apnoea during pregnancy on the
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