Journal of International Obstetrics and Gynecology ›› 2024, Vol. 51 ›› Issue (2): 161-166.doi: 10.12280/gjfckx.20231050

• Obstetric Physiology & Obstetric Disease: Review • Previous Articles     Next Articles

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

WANG Yan, WANG Ya-hui, WANG Yan(), PEI Fei   

  1. Heilongjiang University of Traditional Chinese Medicine, Harbin 150040, China (WANG Yan, WANG Ya-hui); The Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin 150001, China (WANG Yan, PEI Fei)
  • Received:2023-12-14 Published:2024-04-15 Online:2024-04-19
  • Contact: WANG Yan, E-mail: swallow-1113@163.com

Abstract:

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 (TNF-α) 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-α and 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-α and IL-6 may help improve the skeletal muscle development in FGR fetuses. Overall, the role of TNF-α and 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.

Key words: Interleukin-6, Tumor necrosis factor-alpha, Fetal growth retardation, Signal transduction, Muscle, skeletal