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纤维细胞生长因子7通过向线粒体来保护骨质细胞免受氧化损伤

Xiaoyu Liu^1,2,3, Xuchen Hu^1,2,3, Chenguang Niu^1,2,3

¹Department of Endodontics, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|March 11, 2024

概括

纤维细胞生长因子7 (FGF7) 通过提高细胞活力和分化来保护骨质细胞免受氧化应激. FGF7调节活性氧物种并影响关键信号通路,为骨质疏松症提供潜在的治疗策略.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
骨生物学骨生物学骨生物学

背景情况:

骨质疏松病理生理学涉及由于氧化应激而导致骨质母细胞功能受损.
将氧化应激与骨质母细胞功能障碍联系在一起的机制尚未完全理解.

研究的目的:

研究纤维细胞生长因子7 (FGF7) 在氧化应激条件下对骨质细胞行为的影响.
阐明FGF7对过氧化 (H2O2) 诱导的骨质细胞损伤的保护机制.

主要方法:

骨质细胞类MC3T3细胞被预先用复合FGF7进行治疗,并暴露于H2O2诱导的氧化应激.
评估了细胞亡,活力,骨质分化,活性氧物种 (ROS) 水平,线粒体功能和MAPK信号通路 (p38/MAPK,JNK/MAPK).

主要成果:

作为对H2O2.2.的反应,内源性FGF7水平增加.
FGF7治疗显著降低了H2O2诱导的亡,并改善了骨质细胞活力和分化.
FGF7调节了ROS恒温,部分保留了线粒体形态和功能,并调节了p38/MAPK和JNK/MAPK信号.

结论:

FGF7在骨质母细胞中表现出对氧化应激的保护作用.
FGF7通过调节ROS,维护线粒体完整性和影响MAPK信号通路来起作用.
FGF7是一个有前途的治疗候选人,可以保护骨质细胞平衡,并可能治疗骨质疏松症.

关键词:

第七届国家财政基金这就是ROSOS ROS.线粒体中的线粒体.骨质母细胞 (osteoblasts) 是一个骨质细胞.氧化应激是一种氧化应激.

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