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肺损伤与修复：甲醛、褪黑素与Nrf2信号通路相互作用的研究现状
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Abstract:
本文综述了急性肺损伤(acute lung injury, ALI)与修复过程中，甲醛(formaldehyde, FA)、褪黑素(melatonin, MT)和核因子E2相关因子2 (nuclear factor E2-related factor 2, Nrf2)信号通路的相互作用。FA暴露会导致ALI，而MT能够通过调节Nrf2信号通路发挥抗氧化和保护作用。Nrf2信号通路在FA和MT的相互作用中发挥中介作用，共同影响氧化应激和细胞损伤，从而对抗FA对肺组织的损伤，并促进肺损伤的修复。然而，目前的研究仍存在一些局限性和不足，未来可以从多个角度深入研究，为ALI的预防和治疗提供新思路和方法。
This paper reviews the interaction of formaldehyde (FA), melatonin (MT) and nuclear factor E2-related factor 2 (Nrf2) signaling pathways during acute lung injury (ALI) and repair. FA expo-sure leads to ALI, whereas MT can exert antioxidant and protective effects by regulating the Nrf2 signaling pathway, which plays a mediating role in the interaction between FA and MT, and jointly affects oxidative stress and cellular damage, thus counteracting FA damage to lung tissue and pro-moting lung injury repair. However, there are still some limitations and shortcomings in the current study, which can be studied in depth from multiple perspectives in the future to provide new ideas and methods for the prevention and treatment of ALI.
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