骨关节炎
脂肪组织
调解人
肥胖
旁分泌信号
瘦素
内科学
内分泌学
医学
调节器
脂肪生成
炎症
生物
病理
受体
遗传学
基因
替代医学
作者
Kelsey H. Collins,Kristin L. Lenz,Eleanor N. Pollitt,Daniel Ferguson,Irina Hutson,Luke E. Springer,Arin K. Oestreich,Ruhang Tang,Yun Rak Choi,Gretchen A. Meyer,Steven L. Teitelbaum,Christine Pham,Charles Harris,Farshid Guilak
标识
DOI:10.1073/pnas.2021096118
摘要
Osteoarthritis (OA), the leading cause of pain and disability worldwide, disproportionally affects individuals with obesity. The mechanisms by which obesity leads to the onset and progression of OA are unclear due to the complex interactions among the metabolic, biomechanical, and inflammatory factors that accompany increased adiposity. We used a murine preclinical model of lipodystrophy (LD) to examine the direct contribution of adipose tissue to OA. Knee joints of LD mice were protected from spontaneous or posttraumatic OA, on either a chow or high-fat diet, despite similar body weight and the presence of systemic inflammation. These findings indicate that adipose tissue itself plays a critical role in the pathophysiology of OA. Susceptibility to posttraumatic OA was reintroduced into LD mice using implantation of a small adipose tissue depot derived from wild-type animals or mouse embryonic fibroblasts that undergo spontaneous adipogenesis, implicating paracrine signaling from fat, rather than body weight, as a mediator of joint degeneration.
科研通智能强力驱动
Strongly Powered by AbleSci AI