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莱普/PPARγ相互作用调解了类风湿性关节炎中肥胖驱动的Th17分化

Shuang Ren¹, Fanyan Meng¹, Jing Zeng¹

¹Department of Chinese Medicine, National Regional Diagnosis and Treatment Center for TCM Rheumatology, The first Hospital of China Medical University, Shenyang, 110001, Liaoning, China.

Biochimica et biophysica acta. Molecular basis of disease

|October 9, 2025

概括

肥胖问题肥胖问题

科学领域:

免疫学免疫学免疫学
内分泌学在内分泌学.
类风湿病学类风湿病学

背景情况:

类风湿性关节炎 (RA) 是一种慢性自身免疫性疾病,与肥胖有着复杂的关系.
肥胖在RA病理生理学中的作用受到争论,流行病学数据相互矛盾.
了解肥胖和RA相关的分子机制对于向治疗至关重要.

研究的目的:

研究肥胖对类风湿性关节炎 (RA) 进展的影响.
为了阐明阿迪波金勒普丁在RA病变发生中的作用.
为了探索瘦素与过氧酶增殖器激活受体玛 (PPARγ) 和Th17细胞分化之间的相互作用.

主要方法:

在肥胖的RA患者中分析血清勒丁水平.
使用高脂肪饮食 (HFD) 诱导的肥胖和瘦素基因缺陷 (ob) 的小鼠模型.
在各种肥胖模型中研究了原诱导关节炎 (CIA) 和Th17偏振.

主要成果:

在肥胖的RA患者中,血清勒丁水平升高与疾病严重程度相关.
在CIA小鼠中,HFD诱导的肥胖症加剧了关节炎和骨破坏.
瘦素,而不是肥胖本身,通过PPARγ相互作用促进了Th17细胞分化,恶化了RA.

结论:

瘦素是肥胖个体RA进展的关键驱动因素.
莱普与PPARγ的相互作用促进了Th17细胞的分化,从而导致RA的发病.
莱普代表了在肥胖患者中管理RA的潜在治疗标.

关键词:

勒普丁是一种激素.肥胖问题肥胖问题在 PPARγγ 中.类风湿性关节炎类风湿性关节炎类风湿性关节炎在Th17细胞中.

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