Lung aging alters the intrinsic structure of the lung and pulmonary surfactant system and increases the mortality and morbidity due to respiratory diseases in elderly individuals. We hypothesized that lung aging results from an insufficiency of type II alveolar epithelial cells (AECIIs) in the lung tissue. Sirtuin 3 (SIRT3) is a member of the sirtuin family of proteins that promote longevity in many organisms. Increased SIRT3 expression has been linked to an extended life span in humans. Hence, we speculated that the overexpression of SIRT3 may help to ameliorate lung senescence and improve AECII function. AECIIs were isolated from young and old patients with pneumothorax caused by pulmonary bullae. The expression of SIRT3, manganese superoxide dismutase, and catalase, as well as cell function and senescence indicators of young and old AECIIs, was measured before and after SIRT3 overexpression. After SIRT3 overexpression, the aged state of old AECIIs improved, and antiapoptotic activity, proliferation, and secretion were dramatically enhanced. Surfactant protein C (SPC), which is secreted by AECIIs, reduces alveolar surface tension, repairs the alveolar structure, and regulates inflammation. SPC deficiency in patients is associated with increased inflammation and delayed repair. SIRT3 deacetylated forkhead box O3a, thereby protecting mitochondria from oxidative stress and improving cell function and the senescent state of old AECIIs. These findings provide a possible direction for aging-delaying therapies and interventions for diseases of the respiratory system.

中文翻译：

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Sirtuin 3 通过增强 FoxO3a 依赖性抗氧化防御机制改善肺衰老并改善 II 型肺泡上皮细胞功能

肺老化改变了肺和肺表面活性物质系统的内在结构，增加了老年人因呼吸系统疾病引起的死亡率和发病率。我们假设肺老化是由于肺组织中 II 型肺泡上皮细胞 (AECII) 不足所致。Sirtuin 3 (SIRT3) 是 sirtuin 蛋白家族的成员，可促进许多生物体的寿命。增加的 SIRT3 表达与人类寿命延长有关。因此，我们推测 SIRT3 的过表达可能有助于改善肺衰老并改善 AECII 功能。AECII 是从年轻和老年肺大疱引起的气胸患者中分离出来的。SIRT3、锰超氧化物歧化酶、过氧化氢酶的表达，以及年轻和老年AECII的细胞功能和衰老指标，在 SIRT3 过表达之前和之后测量。SIRT3过表达后，老年AECII的衰老状态得到改善，抗凋亡活性、增殖和分泌显着增强。由 AECII 分泌的表面活性剂蛋白 C (SPC) 可降低肺泡表面张力、修复肺泡结构并调节炎症。患者的 SPC 缺乏与炎症增加和修复延迟有关。SIRT3 去乙酰化叉头盒 O3a，从而保护线粒体免受氧化应激并改善细胞功能和旧 AECII 的衰老状态。这些发现为延缓衰老的疗法和呼吸系统疾病的干预提供了可能的方向。和抗凋亡活性、增殖和分泌显着增强。由 AECII 分泌的表面活性剂蛋白 C (SPC) 可降低肺泡表面张力、修复肺泡结构并调节炎症。患者的 SPC 缺乏与炎症增加和修复延迟有关。SIRT3 去乙酰化叉头盒 O3a，从而保护线粒体免受氧化应激并改善细胞功能和旧 AECII 的衰老状态。这些发现为延缓衰老的疗法和呼吸系统疾病的干预提供了可能的方向。和抗凋亡活性、增殖和分泌显着增强。由 AECII 分泌的表面活性剂蛋白 C (SPC) 可降低肺泡表面张力、修复肺泡结构并调节炎症。患者的 SPC 缺乏与炎症增加和修复延迟有关。SIRT3 去乙酰化叉头盒 O3a，从而保护线粒体免受氧化应激并改善细胞功能和旧 AECII 的衰老状态。这些发现为延缓衰老的疗法和呼吸系统疾病的干预提供了可能的方向。患者的 SPC 缺乏与炎症增加和修复延迟有关。SIRT3 去乙酰化叉头盒 O3a，从而保护线粒体免受氧化应激并改善细胞功能和旧 AECII 的衰老状态。这些发现为延缓衰老的疗法和呼吸系统疾病的干预提供了可能的方向。患者的 SPC 缺乏与炎症增加和修复延迟有关。SIRT3 去乙酰化叉头盒 O3a，从而保护线粒体免受氧化应激并改善细胞功能和旧 AECII 的衰老状态。这些发现为延缓衰老的疗法和呼吸系统疾病的干预提供了可能的方向。