Adverse childhood experiences (ACEs) are psychosocial stressors that occur during sensitive developmental windows and are associated with increased lifetime cardiovascular disease (CVD) risk in a dose-dependent manner. Vascular endothelial dysfunction is a pathophysiological mechanism that promotes hypertension and CVD, and may be a mechanism by which ACEs contribute to lifetime CVD risk. We examined whether exposure to ACEs is associated with reduced vascular endothelial function (VEF) in otherwise healthy, young adult women (20.7 ± 3 years) with (ACE+) versus without (ACE-) ACEs, explored whether differences in circulating SIRT1 or systemic oxidative stress could explain ACEs-related differences in VEF, and examined the ability of a pilot, 8-week exercise intervention to augment VEF and SIRT1, or reduce oxidized LDL cholesterol (oxLDL) in ACE+ young adult women. Forty-two otherwise healthy young adults completed this study. Prior to the intervention, VEF (P = 0.002) and SIRT1 (P = 0.004) were lower in the ACE+ than ACE- group, but oxLDL concentrations were not different (P = 0.77). There were also significant associations (P ≤ 0.04) among FMD, SIRT1, and oxLDL in the ACE+, but not ACE- group. Adjusting for circulating SIRT1 and oxLDL reduced the differences in FMD observed between groups (P = 0.10), but only SIRT1 was a significant adjuster of the means (P < 0.05). The exercise intervention employed was unable to enhance VEF or SIRT1 in the ACE+ exercise group. Our data suggest that ACEs likely increase susceptibility to hypertension and CVD via reduced vascular function, perhaps through a SIRT1 pathway-related mechanism.

中文翻译：

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童年社会心理压力与血管内皮功能受损、SIRT1 降低和青年期氧化应激有关

不良童年经历 (ACE) 是发生在敏感发育窗口期间的心理社会压力因素，并以剂量​​依赖性方式与终生心血管疾病 (CVD) 风险增加相关。血管内皮功能障碍是促进高血压和 CVD 的病理生理机制，并且可能是 ACE 导致终生 CVD 风险的机制。我们检查了在其他方面健康的年轻成年女性（20.7 ± 3 岁）有（ACE+）与没有（ACE-）ACE 的情况下，暴露于 ACE 是否与血管内皮功能 (VEF) 降低有关，并探讨了循环 SIRT1 或全身氧化压力可以解释 ACE 相关的 VEF 差异，并检查了试点 8 周运动干预增加 VEF 和 SIRT1 的能力，或降低 ACE+ 年轻女性的氧化 LDL 胆固醇 (oxLDL)。四十二名健康的年轻人完成了这项研究。干预前，ACE+组的VEF（P = 0.002）和SIRT1（P = 0.004）低于ACE-组，但oxLDL浓度没有差异（P = 0.77）。在 ACE+ 组中 FMD、SIRT1 和 oxLDL 之间也存在显着关联（P ≤ 0.04），但在 ACE- 组中没有。调整循环 SIRT1 和 oxLDL 减少了组间观察到的 FMD 差异（P = 0.10），但只有 SIRT1 是平均值的显着调节因子（P < 0.05）。所采用的运动干预无法提高 ACE+ 运动组的 VEF 或 SIRT1。我们的数据表明，ACE 可能通过降低血管功能（可能是通过 SIRT1 通路相关机制）增加对高血压和 CVD 的易感性。