Department of Internal Medicine III and Institute for Clinical Immunology; University of Erlangen-Nuremberg; Erlangen, Germany.
Autophagy. 2013 Aug;9(8):1253-5. doi: 10.4161/auto.25467. Epub 2013 Jun 25.
Autophagy describes the degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery. Autophagy is essentially required to prevent accumulation of cellular damage and to ensure cellular homeostasis. Indeed, impaired autophagy has been implicated in a variety of different diseases. We examined the role of autophagy in inflammatory bone loss. We demonstrated that autophagy is activated by the pro-inflammatory cytokine tumor necrosis factor (TNF/TNFα) in osteoclasts of patients with rheumatoid arthritis (RA). Autophagy induces osteoclast differentiation and stimulates osteoclast-mediated bone resorption in vitro and in vivo, thereby highlighting autophagy as a novel mediator of TNF-induced bone resorption.
自噬描述了通过溶酶体机制降解不必要或功能失调的细胞成分。自噬对于防止细胞损伤积累和确保细胞内稳态是必不可少的。事实上，自噬受损与多种不同的疾病有关。我们研究了自噬在炎症性骨丢失中的作用。我们证明，促炎细胞因子肿瘤坏死因子（TNF/TNFα）在类风湿关节炎（RA）患者的破骨细胞中激活了自噬。自噬诱导破骨细胞分化，并刺激体外和体内破骨细胞介导的骨吸收，从而强调了自噬作为 TNF 诱导的骨吸收的一种新的介质。
