TNF-α和IL-6对胎儿生长受限胎儿骨骼肌的影响

The Effects of TNF-αand IL-6 on Skeletal Muscle of Fetuses with Fetal Growth Restriction

胎儿生长受限(fetal growth restriction,FGR)是一种常见的产科疾病,其可导致新生儿低出生体质量和出生后肌肉量减少。这可能与肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白细胞介素-6(interleukin-6,IL-6)的调控密切相关。研究发现,这两种炎症因子在FGR胎儿中表达水平异常,可通过影响成肌细胞的增殖和分化,干扰正常骨骼肌的发育。此外,TNF-α与IL-6还可以激活特定的信号通路,如核因子κB(nuclear factor-κB,NF-κB)、Janus激酶/信号转导及转录活化因子(Janus kinase/signal transducer and activator of transcription,JAK/STAT)、丝裂原激活的蛋白激酶(mitogen-activated protein kinase,MAPK)等信号通路,调节肌细胞的代谢和功能。如使用特定的抗炎药物或生物制剂来降低TNF-α和IL-6的活性,可能有助于改善FGR胎儿的骨骼肌发育。总的来说,TNF-α和IL-6在FGR胎儿骨骼肌发育中的作用是一个多层面、复杂的过程,需要进一步的深入研究来阐明其具体机制,帮助理解FGR的病理生理学,并为治疗FGR胎儿提供新的思路。

Fetal growth restriction(FGR)is a common obstetric condition and resulting in low birth weight and reduced muscle mass in newborns after birth.This may be closely related to the regulatory mechanisms of tumor necrosis factor-α(TNFα)and interleukin-6(IL-6).Studies have found that these two inflammatory factors are expressed at abnormal levels in FGR fetuses,affecting the proliferation and differentiation of myoblasts,interfering with the normal development of skeletal muscle.Moreover,TNF-αand IL-6 can activate specific signaling pathways,such as nuclear factor-κB(NF-κB),Janus kinase/signal transducer and activator of transcription(JAK/STAT),mitogen-activated protein kinase(MAPK),and other signaling pathways that regulate myocyte metabolism and function.Using specific anti-inflammatory drugs or biological agents to reduce the activity of TNF-αand IL-6 may help improve the skeletal muscle development in FGR fetuses.Overall,the role of TNF-αand IL-6 in the skeletal muscle development of FGR fetuses is a multifaceted and complex process,requiring further in-depth research to clarify their specific mechanisms,aiding to the understanding of the pathophysiology of FGR,and providing new ideas for the treatment of FGR fetuses.