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Role of the Renin-Angiotensin System in PM2.5-Induced Lung Injury: A Mini-review

腎素-血管收縮素系統在空氣汙染物PM2.5引發肺損傷中的角色:一個小型綜論

摘要


Air pollution has worsened in recent decades and is known to adversely affect the human respiratory and circulatory systems. Many studies have shown that some constituents of polluted air can trigger or aggravate respiratory and cardiac diseases by inducing lung injury through PM2.5-induced cytokine release and oxidative stress. To review recent findings regarding the effects of fine particles with an aerodynamic diameter of 2.5 μm or less (PM2.5) on lung injury, searches on the Cochrane Library, PubMed, and Google Scholar were performed using keywords "PM2.5," "air pollution," "lung injury," "renin-angiotensin system," and others. The relationships among these effects, including the renin-angiotensin system, and the lack of angiotensin-converting enzyme II were discussed. The involvement of the angiotensin-converting enzyme II-angiotensin-(1-7)-Mas axis in the regulation of inflammatory processes and the context of lung inflammation and fibrosis was reviewed. Recent studies have provided some clarity regarding the mechanisms underlying PM2.5-induced lung injury, which may aid in the development of novel treatments for PM2.5-related pulmonary diseases and injuries.

並列摘要


背景:近幾十年來普遍惡化的空氣汙染已是被公認為造成呼吸道及循環系統問題的主要原因。目的:過去的研究已經發現粒徑小於或等於2.5μm的懸浮微粒和肺損傷有莫大的相關性,而可能的原因又與腎素-血管收縮素系統及缺乏第二型血管收縮素轉化酶有關。方法:文獻回顧的方式採用搜尋Cochrane Library, PubMed, and Google Scholar等系統的方式,搜尋地的關鍵字為空氣汙染、PM2.5肺損傷及腎素-血管收縮素系統等。主要結果與結論:現存的文獻明確的提供一些有關腎素-血管收縮素系統在PM2.5導致肺損傷中所扮演的角色及機制,希望藉由這些證據有助於發展針對PM2.5有關的肺病與肺損傷的全新的療法。

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