Scholarlink

Background <p>Cancer cachexia is a multifactorial metabolic syndrome marked by progressive skeletal muscle wasting, systemic inflammation, reduced quality of life, and poor clinical outcomes. Interleukin-6 (IL-6) is a central mediator in cachexia pathophysiology, driving inflammatory signaling, catabolic metabolism, and muscle atrophy. However, IL-6 also rises transiently during exercise, where it exerts beneficial metabolic and anti-inflammatory effects, highlighting the context-dependent nature of IL-6 signaling.</p> Main body <p>This review summarizes current knowledge on the regulation and function of IL-6 in cancer cachexia and examines how exercise training modulates IL-6 production and downstream signaling pathways. We focus on the mechanistic differences between chronic, tumor-derived IL-6 and acute, exercise-induced IL-6, particularly their divergent effects on the JAK/STAT3, NF-κB, and AMPK cascades. In addition, we review preclinical and clinical evidence demonstrating that exercise can attenuate cachexia by reprogramming inflammatory responses, preserving skeletal muscle mass, and improving metabolic homeostasis.</p> Conclusions <p>Accumulating evidence indicates that structured exercise interventions may represent a promising non-pharmacological adjunct to counteract IL-6-driven cancer cachexia and improve patient outcomes. Future research should aim to optimize exercise prescriptions and explore potential synergistic effects between exercise and IL-6-targeted therapies to enhance therapeutic efficacy in cachectic cancer patients.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Exercise-modulated IL-6 in cancer cachexia: molecular mechanisms and therapeutic potential

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月12日

查看全文
  • Shujuan Wei,
  • Xinyi Lv,
  • Yiming Xu,
  • Shengguang Ding

摘要

Background

Cancer cachexia is a multifactorial metabolic syndrome marked by progressive skeletal muscle wasting, systemic inflammation, reduced quality of life, and poor clinical outcomes. Interleukin-6 (IL-6) is a central mediator in cachexia pathophysiology, driving inflammatory signaling, catabolic metabolism, and muscle atrophy. However, IL-6 also rises transiently during exercise, where it exerts beneficial metabolic and anti-inflammatory effects, highlighting the context-dependent nature of IL-6 signaling.

Main body

This review summarizes current knowledge on the regulation and function of IL-6 in cancer cachexia and examines how exercise training modulates IL-6 production and downstream signaling pathways. We focus on the mechanistic differences between chronic, tumor-derived IL-6 and acute, exercise-induced IL-6, particularly their divergent effects on the JAK/STAT3, NF-κB, and AMPK cascades. In addition, we review preclinical and clinical evidence demonstrating that exercise can attenuate cachexia by reprogramming inflammatory responses, preserving skeletal muscle mass, and improving metabolic homeostasis.

Conclusions

Accumulating evidence indicates that structured exercise interventions may represent a promising non-pharmacological adjunct to counteract IL-6-driven cancer cachexia and improve patient outcomes. Future research should aim to optimize exercise prescriptions and explore potential synergistic effects between exercise and IL-6-targeted therapies to enhance therapeutic efficacy in cachectic cancer patients.