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A mechanistic look at the effects of adversity early in life on cardiovascular disease risk during adulthood

机译:机械观察生命早期逆境对成年期间心血管疾病风险的影响

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摘要

Early origins of adult disease may be defined as adversity or challenges during early life that alter physiological responses and prime the organism to chronic disease in adult life. Adverse childhood experiences or early life stress (ELS) may be considered a silent independent risk factor capable of predicting future cardiovascular disease risk. Maternal separation (Mat-Sep) provides a suitable model to elucidate the underlying molecular mechanisms by which ELS increases the risk to develop cardiovascular disease in adulthood. The aim of this review is to describe the links between behavioural stress early in life and chronic cardiovascular disease risk in adulthood. We will discuss the following: (i) adult cardiovascular outcomes in humans subjected to ELS, (ii) Mat-Sep as an animal model of ELS as well as the limitations and advantages of this model in rodents and (iii) possible ELS-induced mechanisms that predispose individuals to greater cardiovascular risk. Overall, exposure to a behavioural stressor early in life sensitizes the response to a second stressor later in life, thus unmasking an exaggerated cardiovascular dysfunction that may influence quality of life and life expectancy in adulthood.
机译:成人疾病的早期起源可定义为生命早期的逆境或挑战,这些挑战或挑战改变了生理反应,并使生物体在成人生活中引发了慢性疾病。不良的童年经历或早期生活压力(ELS)可被视为能够预测未来心血管疾病风险的沉默独立危险因素。产妇分离(Mat-Sep)提供了一个合适的模型,以阐明潜在的分子机制,从而使ELS增加成人患心血管疾病的风险。这篇综述的目的是描述生命早期的行为压力与成年后慢性心血管疾病风险之间的联系。我们将讨论以下内容:(i)患有ELS的人类的成人心血管结局,(ii)Mat-Sep作为ELS的动物模型,以及该模型在啮齿动物中的局限性和优势,以及(iii)可能由ELS引起的使个体更易罹患心血管疾病的机制。总体而言,在生命早期接触行为应激源会使对生命后期第二应激源的反应敏感,从而掩盖了可能影响生活质量和成年预期寿命的夸大心血管功能障碍。

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