Front Physiol:ROS和自噬之间的潜在联系参与了牙周炎的发病机制

2017-07-17 MedSci MedSci原创

牙周炎是一种慢性炎症性疾病,可导致牙周支持组织(牙龈、牙周膜和牙槽骨)的破坏。牙周组织破坏的主要原因是宿主对微生物及其毒性产物的免疫反应。具体而言,活性氧(ROS)和抗氧化防御系统之间失衡与牙周炎的发病机制有关。作为细胞内信号转导者,ROS水平的升高可导致自噬,这在牙周炎中通过促进细胞死亡或阻断感染细胞的凋亡中起着双重作用。自噬还可以调节ROS的产生和清除。为阐明ROS与自噬之间的串扰机制,已有多

牙周炎是一种慢性炎症性疾病,可导致牙周支持组织(牙龈、牙周膜和牙槽骨)的破坏。

牙周组织破坏的主要原因是宿主对微生物及其毒性产物的免疫反应。具体而言,活性氧(ROS)和抗氧化防御系统之间失衡与牙周炎的发病机制有关。作为细胞内信号转导者,ROS水平的升高可导致自噬,这在牙周炎中通过促进细胞死亡或阻断感染细胞的凋亡中起着双重作用。自噬还可以调节ROS的产生和清除。

为阐明ROS与自噬之间的串扰机制,已有多个研究正在进行。这里,本文综述了ROS和自噬在牙周组织中的生理及病理作用。对自噬相关的氧化还原敏感通路,如mTORC1,Beclin 1,和ATG12-ATG5复合体,进行了深入探讨以了解ROS和自噬之间的串扰。结果发现,根据目前的证据,研究人员认为ROS和自噬之间的潜在联系参与了牙周炎的发病机制。

原始出处:

Chengcheng Liu, Longyi Mo, et al., The Role of Reactive Oxygen Species and Autophagy in Periodontitis and Their Potential Linkage. Front Physiol. 2017; 8: 439. Published online 2017 Jun 23. doi: 10.3389/fphys.2017.00439.

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    2017-07-19 lsndxfj
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    2017-07-18 changjiu

    学习了,谢谢

    0

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