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Dec1 和 Dec2 在牙周炎炎症中的潜在作用。

The Potential Roles of Dec1 and Dec2 in Periodontal Inflammation.

机构信息

Department of Biochemistry, Nihon University School of Medicine, Tokyo 173-8610, Japan.

Pathology Division, Shizuoka Cancer Center, Shizuoka 411-8777, Japan.

出版信息

Int J Mol Sci. 2021 Sep 26;22(19):10349. doi: 10.3390/ijms221910349.

DOI:10.3390/ijms221910349
PMID:34638690
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8508764/
Abstract

Periodontal inflammation is a common inflammatory disease associated with chronic inflammation that can ultimately lead to alveolar attachment loss and bone destruction. Understanding autophagy and pyroptosis has suggested their significant roles in inflammation. In recent years, studies of differentiated embryo-chondrocyte expressed genes 1 and 2 (Dec1 and Dec2) have shown that they play important functions in autophagy and in pyroptosis, which contribute to the onset of periodontal inflammation. In this review, we summarize recent studies on the roles of clock genes, including Dec1 and Dec2, that are related to periodontal inflammation and other diseases.

摘要

牙周炎是一种常见的炎症性疾病,与慢性炎症有关,最终可导致牙槽附着丧失和骨破坏。自噬和细胞焦亡的研究表明它们在炎症中具有重要作用。近年来,分化胚胎软骨细胞表达基因 1 和 2(Dec1 和 Dec2)的研究表明,它们在自噬和细胞焦亡中发挥重要作用,从而导致牙周炎的发生。本综述总结了与牙周炎和其他疾病相关的时钟基因(包括 Dec1 和 Dec2)在牙周炎中的作用的最新研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0cf/8508764/5b8517ab4a56/ijms-22-10349-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0cf/8508764/84caae60950e/ijms-22-10349-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0cf/8508764/5b8517ab4a56/ijms-22-10349-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0cf/8508764/84caae60950e/ijms-22-10349-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0cf/8508764/5b8517ab4a56/ijms-22-10349-g002.jpg

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A deficiency of Dec2 triggers periodontal inflammation and pyroptosis.Dec2 缺乏会引发牙周炎和细胞焦亡。
J Periodontal Res. 2021 Jun;56(3):492-500. doi: 10.1111/jre.12849. Epub 2021 Feb 28.
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Loss of Dec1 prevents autophagy in inflamed periodontal ligament fibroblast.Dec1 的缺失阻止了炎症性牙周膜成纤维细胞的自噬。
Bhlhe40 缺乏通过防止巨噬细胞焦亡来减轻 LPS 诱导的急性肺损伤。
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Basic-helix-loop-helix family member e41 suppresses osteoclastogenesis and abnormal bone resorption disease via NFATc1.碱性螺旋-环-螺旋家族成员e41通过活化T细胞核因子c1抑制破骨细胞生成和异常骨吸收疾病。
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Loss of Dec1 inhibits alcohol-induced hepatic lipid accumulation and circadian rhythm disorder.Dec1 的缺失抑制酒精诱导的肝脏脂质积累和昼夜节律紊乱。
BMC Mol Cell Biol. 2024 Jan 2;25(1):1. doi: 10.1186/s12860-023-00497-y.
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