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血管衰老的胎儿起源

Fetal origin of vascular aging.

作者信息

Pitale Shailesh, Sahasrabuddhe Anagha

机构信息

Consultant Endocrinologist, Pitale Diabetes and Hormone Center, Shriman Complex, Dhantoli, India.

出版信息

Indian J Endocrinol Metab. 2011 Oct;15 Suppl 4(Suppl4):S289-97. doi: 10.4103/2230-8210.86971.

DOI:10.4103/2230-8210.86971
PMID:22145131
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3230090/
Abstract

Aging is increasingly regarded as an independent risk factor for development of cardiovascular diseases such as atherosclerosis and hypertension and their complications (e.g. MI and Stroke). It is well known that vascular disease evolve over decades with progressive accumulation of cellular and extracellular materials and many inflammatory processes. Metabolic syndrome, obesity and diabetes are conventionally recognized as risk factors for development of coronary vascular disease (CVD). These conditions are known to accelerate ageing process in general and vascular ageing in particular. Adverse events during intrauterine life may programme organ growth and favour disease later in life, popularly known as, 'Barker's Hypothesis'. The notion of fetal programming implies that during critical periods of prenatal growth, changes in the hormonal and nutritional milieu of the conceptus may alter the full expression of the fetal genome, leading to permanent effects on a range of physiological.

摘要

衰老越来越被视为心血管疾病(如动脉粥样硬化和高血压)及其并发症(如心肌梗死和中风)发生发展的独立危险因素。众所周知,血管疾病会在数十年间随着细胞和细胞外物质的逐渐积累以及许多炎症过程而演变。代谢综合征、肥胖症和糖尿病传统上被认为是冠状动脉疾病(CVD)发生发展的危险因素。众所周知,这些情况通常会加速衰老过程,尤其是血管衰老。子宫内生活期间的不良事件可能会影响器官生长,并增加日后患病的几率,这就是著名的“巴克假说”。胎儿编程的概念意味着,在产前生长的关键时期,胚胎激素和营养环境的变化可能会改变胎儿基因组的充分表达,从而对一系列生理功能产生永久性影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d2/3230090/e050c22b6478/IJEM-15-289-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d2/3230090/08b1850d7260/IJEM-15-289-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d2/3230090/e050c22b6478/IJEM-15-289-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d2/3230090/08b1850d7260/IJEM-15-289-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43d2/3230090/e050c22b6478/IJEM-15-289-g002.jpg

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