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焦磷酸钙沉积病实验小鼠模型的转化价值。

The translational value of calcium pyrophosphate deposition disease experimental mouse models.

作者信息

Luisetto Roberto, Scanu Anna

机构信息

Experimental Surgery Research Center, Department of Surgery, Oncology and Gastroenterology-DISCOG, University of Padova, Padova, Italy.

Department of Women's and Children's Health-SDB, University of Padova, Padova, Italy.

出版信息

Front Med (Lausanne). 2024 May 23;11:1417318. doi: 10.3389/fmed.2024.1417318. eCollection 2024.

Abstract

The deposition of calcium pyrophosphate (CPP) crystals in joint tissues causes acute and chronic arthritis that commonly affect the adult and elderly population. Experimental calcium pyrophosphate deposition disease (CPPD) models are divided into genetically modified models and crystal-induced inflammation models. The former do not reproduce phenotypes overlapping with the human disease, while in the latter, the direct injection of crystals into the ankles, dorsal air pouch or peritoneum constitutes a useful and reliable methodology that resembles the CPP induced-inflammatory condition in humans. The translational importance of the induced model is also strengthened by the fact that the key molecular and cellular mediators involved in inflammation are shared between humans and laboratory rodents. Although, models are indispensable tools for studying the pathogenesis of the CPPD and testing new therapies, their development is still at an early stage and major efforts are needed to address this issue. Here, we analyze the strenghts and limitations of each currently available CPPD model, and critically discuss their translational value.

摘要

焦磷酸钙(CPP)晶体在关节组织中的沉积会引发急性和慢性关节炎,这在成年人和老年人群中较为常见。实验性焦磷酸钙沉积病(CPPD)模型分为基因改造模型和晶体诱导炎症模型。前者无法再现与人类疾病重叠的表型,而在后者中,将晶体直接注射到脚踝、背部气囊或腹膜中是一种有用且可靠的方法,类似于人类中CPP诱导的炎症状态。人类和实验啮齿动物之间共享参与炎症的关键分子和细胞介质这一事实,也增强了诱导模型的转化重要性。尽管模型是研究CPPD发病机制和测试新疗法不可或缺的工具,但其发展仍处于早期阶段,需要付出巨大努力来解决这一问题。在此,我们分析了每种现有CPPD模型的优势和局限性,并批判性地讨论了它们的转化价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f88/11153760/5fccb444d330/fmed-11-1417318-g001.jpg

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