文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

脂多糖（LPS）诱导的自噬负责增强破骨细胞生成。

Lipopolysaccharide (LPS)-Induced Autophagy Is Responsible for Enhanced Osteoclastogenesis.

机构信息

Department of Biological Sciences, University of Ulsan, Ulsan 44610, Korea.

出版信息

Mol Cells. 2017 Nov 30;40(11):880-887. doi: 10.14348/molcells.2017.0230. Epub 2017 Nov 16.

DOI:10.14348/molcells.2017.0230
PMID:29145718
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5712518/
Abstract

We hypothesized that inflammation affects number and activity of osteoclasts (OCs) via enhancing autophagy. Lipopolysaccharide (LPS) induced autophagy, osteoclastogenesis, and cytoplasmic reactive oxygen species (ROS) in bone marrow-derived macrophages that were pre-stimulated with receptor activator of nuclear factor-κB ligand. An autophagy inhibitor, 3-methyladenine (3-MA) decreased LPS-induced OC formation and bone resorption, indicating that autophagy is responsible for increasing number and activity of OCs upon LPS stimulus. Knockdown of autophagy-related protein 7 attenuated the effect of LPS on OC-specific genes, supporting a role of LPS as an autophagy inducer in OC. Removal of ROS decreased LPS-induced OC formation as well as autophagy. However, 3-MA did not affect LPS-induced ROS levels, suggesting that ROS act upstream of phosphatidylinositol-4,5-bisphosphate 3-kinase in LPS-induced autophagy. Our results suggest the possible use of autophagy inhibitors targeting OCs to reduce inflammatory bone loss.

摘要

我们假设炎症通过增强自噬作用来影响破骨细胞（OCs）的数量和活性。脂多糖（LPS）诱导核因子-κB 配体受体激活剂预处理的骨髓来源巨噬细胞中的自噬、破骨细胞生成和细胞质活性氧（ROS）。自噬抑制剂 3-甲基腺嘌呤（3-MA）降低 LPS 诱导的 OC 形成和骨吸收，表明自噬负责增加 LPS 刺激时 OC 的数量和活性。自噬相关蛋白 7 的敲低减弱了 LPS 对 OC 特异性基因的作用，支持 LPS 作为 OC 中自噬诱导剂的作用。去除 ROS 也降低了 LPS 诱导的 OC 形成和自噬。然而，3-MA 不影响 LPS 诱导的 ROS 水平，表明 ROS 在 LPS 诱导的自噬中位于磷脂酰肌醇-4,5-二磷酸 3-激酶的上游。我们的结果表明，针对 OC 的自噬抑制剂可能被用于减少炎症性骨丢失。

相似文献

[1]
Lipopolysaccharide (LPS)-Induced Autophagy Is Responsible for Enhanced Osteoclastogenesis.

Mol Cells. 2017-11-16

[2]
N-Acetylcysteine Attenuates Lipopolysaccharide-Induced Osteolysis by Restoring Bone Remodeling Balance via Reduction of Reactive Oxygen Species Formation During Osteoclastogenesis.

Inflammation. 2020-8

[3]
Autophagy negative-regulating Wnt signaling enhanced inflammatory osteoclastogenesis from Pre-OCs in vitro.

Biomed Pharmacother. 2020-6

[4]
Lycorine Attenuates Autophagy in Osteoclasts via an Axis of mROS/TRPML1/TFEB to Reduce LPS-Induced Bone Loss.

Oxid Med Cell Longev. 2019-10-8

[5]
4-Phenylbutyric acid protects against lipopolysaccharide-induced bone loss by modulating autophagy in osteoclasts.

Biochem Pharmacol. 2018-2-16

[6]
The polymethoxy flavonoid sudachitin suppresses inflammatory bone destruction by directly inhibiting osteoclastogenesis due to reduced ROS production and MAPK activation in osteoclast precursors.

PLoS One. 2018-1-17

[7]
Anti-inflammatory, anti-osteoclastic, and antioxidant activities of genistein protect against alveolar bone loss and periodontal tissue degradation in a mouse model of periodontitis.

J Biomed Mater Res A. 2017-6-6

[8]
Dihydroartemisinin attenuates lipopolysaccharide-induced osteoclastogenesis and bone loss via the mitochondria-dependent apoptosis pathway.

Cell Death Dis. 2016-3-31

[9]
Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy.

Bone. 2015-10

[10]
Monotropein Protects against Inflammatory Bone Loss and Suppresses Osteoclast Formation and Bone Resorption by Inhibiting NFATc1 via NF-κB and Akt/GSK-3β Pathway.

Nutrients. 2022-9-24

引用本文的文献

[1]
Fludarabine attenuates inflammation and dysregulated autophagy in alveolar macrophages via inhibition of STAT1/IRF1 pathway.

Lab Anim Res. 2025-5-7

[2]
Zoledronic Acid Inhibits Lipopolysaccharide-Induced Osteoclastogenesis by Suppressing Macrophage NLRP3-Mediated Autophagy Pathway.

Immun Inflamm Dis. 2024-12

[3]
The role of autophagy in SIM mediated anti-inflammatory osteoclastogenesis through NLRP3 signaling pathway.

Immun Inflamm Dis. 2024-1

[4]
Interleukin-19 promotes bone resorption by suppressing osteoprotegerin expression in BMSCs in a lipopolysaccharide-induced bone loss mouse model.

Bone Joint Res. 2023-11-3

[5]
Low-dose lipopolysaccharide inhibits spinal cord injury-induced neuronal apoptosis by regulating autophagy through the lncRNA MALAT1/Nrf2 axis.

PeerJ. 2023

[6]
Autophagy in Bone Remodeling: A Regulator of Oxidative Stress.

Front Endocrinol (Lausanne). 2022

[7]
Morin Disrupts Cytoskeleton Reorganization in Osteoclasts through an ROS/SHP1/c-Src Axis and Grants Protection from LPS-Induced Bone Loss.

Antioxidants (Basel). 2022-5-12

[8]
Boosting NAD+ blunts TLR4-induced type I IFN in control and systemic lupus erythematosus monocytes.

J Clin Invest. 2022-3-1

[9]
L. reuteri ZJ617 inhibits inflammatory and autophagy signaling pathways in gut-liver axis in piglet induced by lipopolysaccharide.

J Anim Sci Biotechnol. 2021-10-13

[10]
LPS-induced autophagy in human dental pulp cells is associated with p38.

J Mol Histol. 2021-10

本文引用的文献

[1]
Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy.

Bone. 2015-10

[2]
Measuring autophagy in stressed cells.

Methods Mol Biol. 2015

[3]
Inhibition of microtubule dynamics affects podosome belt formation during osteoclast induction.

Cell Biochem Biophys. 2015-3

[4]
Peroxiredoxin II negatively regulates lipopolysaccharide-induced osteoclast formation and bone loss via JNK and STAT3.

Antioxid Redox Signal. 2015-1-1

[5]
Reactive oxygen species induce the association of SHP-1 with c-Src and the oxidation of both to enhance osteoclast survival.

Am J Physiol Endocrinol Metab. 2014-5-13

[6]
Chloroquine reduces osteoclastogenesis in murine osteoporosis by preventing TRAF3 degradation.

J Clin Invest. 2013-12-9

[7]
Autophagy regulates TNFα-mediated joint destruction in experimental arthritis.

Ann Rheum Dis. 2012-9-12

[8]
Microtubule-associated protein light chain 3 regulates Cdc42-dependent actin ring formation in osteoclast.

Int J Biochem Cell Biol. 2012-3-23

[9]
Autophagy proteins regulate the secretory component of osteoclastic bone resorption.

Dev Cell. 2011-11-4

[10]
Osteoclast precursor differentiation by MCPIP via oxidative stress, endoplasmic reticulum stress, and autophagy.

J Mol Cell Biol. 2011-10-11

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索