介导的咖啡因代谢涉及骨关节炎中破骨细胞的铁死亡。

-mediated caffeine metabolism involves ferroptosis of osteoblasts in osteoarthritis.

作者信息

Li Feng, Wen Xin, Xue Pu, Xu Huiping, Wu Panyang, Xu Zhiming, Wang Xianwei, Pi Guofu

机构信息

Department of Orthopedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Department of Orthopedics, People's Hospital of Zhengzhou, Zhengzhou, China.

出版信息

Microbiol Spectr. 2025 Jun 3;13(6):e0157524. doi: 10.1128/spectrum.01575-24. Epub 2025 Apr 24.

Abstract

There is a positive causality between coffee consumption and osteoarthritis (OA); however, whether gut microbiota is involved needs to be discussed. Here, we observed that in caffeine consumers, fecal abundance was positively correlated with subchondral bone mass, serum caffeine concentration was negatively correlated with bone mass, and fecal was negatively correlated with serum caffeine. In the OA model, caffeine intake aggravated articular cartilage destruction, bone mass loss, and intestinal barrier damage; on the contrary, paraxanthine intake reversed the above lesions. Importantly, after the intestinal supplement, caffeine-induced lesions in OA mice were effectively alleviated. Mechanically, has the potential to metabolize caffeine into paraxanthine, and this effect could alleviate the ferroptosis of osteoblast in the OA model. This study screened out that an endogenous bacteria, has the ability to metabolize caffeine and revealed its effects on OA progression.IMPORTANCEThere is positive causality between coffee consumption and osteoarthritis (OA). Caffeine exposure is responsible for the reduction of bone mass and restrained osteoblast function. abundance is exhausted in gut and positively correlated with subchondral bone mass in coffee consumption patients with OA. Supplement of intestinal alleviates caffeine-induced subchondral bone loss. has the potential to metabolize caffeine into paraxanthine, and this effect alleviates ferroptosis of osteoblast. Our study illustrated that intestinal possibly serves as a novel promising treatment for coffee consumers with OA.

摘要

咖啡消费与骨关节炎(OA)之间存在正向因果关系;然而,肠道微生物群是否参与其中仍有待探讨。在此,我们观察到,在饮用咖啡因的人群中,粪便[某种细菌名称]丰度与软骨下骨量呈正相关,血清咖啡因浓度与骨量呈负相关,且粪便[某种细菌名称]与血清咖啡因呈负相关。在OA模型中,摄入咖啡因会加重关节软骨破坏、骨量流失和肠道屏障损伤;相反,摄入副黄嘌呤可逆转上述病变。重要的是,补充肠道[某种细菌名称]后,咖啡因诱导的OA小鼠病变得到有效缓解。从机制上讲,[某种细菌名称]有将咖啡因代谢为副黄嘌呤的潜力,且这种作用可减轻OA模型中成骨细胞的铁死亡。本研究筛选出[某种细菌名称]这种内源性细菌具有代谢咖啡因的能力,并揭示了其对OA进展的影响。

重要性

咖啡消费与骨关节炎(OA)之间存在正向因果关系。咖啡因暴露会导致骨量减少和成骨细胞功能受限。在患有OA的咖啡消费人群中,肠道内[某种细菌名称]丰度降低,且与软骨下骨量呈正相关。补充肠道[某种细菌名称]可减轻咖啡因诱导的软骨下骨丢失。[某种细菌名称]有将咖啡因代谢为副黄嘌呤的潜力,且这种作用可减轻成骨细胞的铁死亡。我们的研究表明,肠道[某种细菌名称]可能是治疗患有OA的咖啡消费者的一种新的有前景的疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a8/12131801/4c90dc98da3b/spectrum.01575-24.f001.jpg

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