Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041. China.
Collaborative Innivation Centre of Biotherapy and Cancer Centre, West China Hospital, Sichuan University, No. 37 Guoxue Xiang, Chengdu. China.
Curr Drug Targets. 2017;18(14):1664-1675. doi: 10.2174/1389450118666170104153512.
Obesity was traditionally considered as a positive regulator on the strength of bone. With the in-depth study, obesity is considered as a major risk factor for osteoporosis. Some proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) are the factors that fat uses to negatively regulate bone metabolism.
This review was aimed to summarize and critically discuss the convincing evidence for the therapeutic effectiveness of pro-inflammatory cytokines for the treatment of obesity-related bone disorders.
Obese people and animals show a higher level of serum TNF-α and IL-6, which are produced by macrophages derived from adipose tissue. These pro-inflammatory cytokines regulate the proliferation and apoptosis of adipocyte, promote lipolysis, inhibit lipid synthesis and decrease blood lipids through autocrine and paracrine way. On the other hand, TNF-α and IL-6 regulate bone metabolism through the endocrine way. Several reports suggest that TNF-α is a negative regulator of osteoblast at some stages of differentiation and positively regulates osteoclast proliferation and differentiation. In contrast, IL-6 influences osteoblasts and osteoclasts through complex mechanisms, which reflect dual effects. In addition, TNF-α and IL-6 may regulate bone metabolism indirectly by regulating adiponectin and leptin released from adipocytes.
In this review, we first summarize the role of TNF-α and IL-6 in lipid and bone metabolisms. We further discuss how TNF-α and IL-6 regulate the communication between fat and bone, and their pathological roles in obesity-related bone disorders. Lastly, we discuss the possibility of using pro-inflammatory signaling pathway as a therapeutic target to develop drug for obesity-related bone disorders.
肥胖传统上被认为是骨骼强度的正向调节剂。随着深入研究,肥胖被认为是骨质疏松症的主要危险因素。一些促炎细胞因子,如肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6),是脂肪用来负向调节骨代谢的因素。
本综述旨在总结和批判性讨论促炎细胞因子治疗肥胖相关骨疾病的治疗效果的有力证据。
肥胖者和动物表现出更高水平的血清 TNF-α和 IL-6,这些细胞因子由脂肪组织来源的巨噬细胞产生。这些促炎细胞因子通过自分泌和旁分泌方式调节脂肪细胞的增殖和凋亡,促进脂肪分解,抑制脂质合成并降低血脂。另一方面,TNF-α和 IL-6 通过内分泌方式调节骨代谢。一些报道表明,TNF-α在某些分化阶段是成骨细胞的负向调节剂,并且正向调节破骨细胞的增殖和分化。相比之下,IL-6 通过复杂的机制影响成骨细胞和破骨细胞,反映出双重作用。此外,TNF-α和 IL-6 可能通过调节脂肪细胞释放的脂联素和瘦素来间接调节骨代谢。
在本综述中,我们首先总结了 TNF-α和 IL-6 在脂质和骨代谢中的作用。我们进一步讨论了 TNF-α和 IL-6 如何调节脂肪和骨骼之间的通讯,以及它们在肥胖相关骨疾病中的病理作用。最后,我们讨论了利用促炎信号通路作为治疗肥胖相关骨疾病的药物靶点的可能性。