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<p>Macrophage polarization refers to the process by which macrophages exhibit different functional states in response to various microenvironmental stimuli, primarily classified into pro-inflammatory M1 type and anti-inflammatory M2 type. In recent years, with the development of tumor immunology, the role of macrophage polarization in the tumor microenvironment has gradually become a research hotspot, especially showing significant impacts on the occurrence, development, and immune evasion mechanisms of cervical cancer. Recent studies have shown that tumor-associated macrophages (TAMs) significantly influence tumor progression, immune suppression, and resistance to radiotherapy by transitioning to different polarization states, particularly toward M2 polarization. The dynamic balance between the two is crucial for the progression of cervical cancer. However, the specific regulatory mechanisms of macrophage polarization and its interactions with other immune cells in the tumor microenvironment still leave many puzzles unsolved. This article aims to systematically review the research progress in macrophage polarization in the field of cervical cancer treatment in recent years, with a focus on three core directions. First, we will summarize the novel subsets and functional programs of TAMs in cervical cancer revealed by advanced technologies such as modern single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics. These high-resolution technologies can go beyond the traditional M1/M2 dichotomy to identify macrophage subsets with unique gene expression profiles and functions at specific spatial locations, thereby providing a basis for developing more precise targeted strategies. Second, we will delve into the mechanisms of macrophage recruitment and immune evasion driven by HPV infection and tumor hypoxia, supported by strong original experimental evidence. Finally, this review will critically evaluate the practical translational potential of various current therapeutic strategies targeting TAMs. It provides new perspectives for understanding the immune microenvironment of cervical cancer and lays the foundation for optimizing clinical treatment strategies and developing novel immune-targeted therapies.</p>

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The role of macrophage polarization in cervical cancer and its potential therapeutic targets

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月29日

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  • Feixia Li,
  • Gang Tian,
  • Yan Ding,
  • Jing Cui,
  • Jiaojiao Zhu,
  • Xiaoying Chang,
  • Tuoyang Hu,
  • Yucun Wang

摘要

Macrophage polarization refers to the process by which macrophages exhibit different functional states in response to various microenvironmental stimuli, primarily classified into pro-inflammatory M1 type and anti-inflammatory M2 type. In recent years, with the development of tumor immunology, the role of macrophage polarization in the tumor microenvironment has gradually become a research hotspot, especially showing significant impacts on the occurrence, development, and immune evasion mechanisms of cervical cancer. Recent studies have shown that tumor-associated macrophages (TAMs) significantly influence tumor progression, immune suppression, and resistance to radiotherapy by transitioning to different polarization states, particularly toward M2 polarization. The dynamic balance between the two is crucial for the progression of cervical cancer. However, the specific regulatory mechanisms of macrophage polarization and its interactions with other immune cells in the tumor microenvironment still leave many puzzles unsolved. This article aims to systematically review the research progress in macrophage polarization in the field of cervical cancer treatment in recent years, with a focus on three core directions. First, we will summarize the novel subsets and functional programs of TAMs in cervical cancer revealed by advanced technologies such as modern single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics. These high-resolution technologies can go beyond the traditional M1/M2 dichotomy to identify macrophage subsets with unique gene expression profiles and functions at specific spatial locations, thereby providing a basis for developing more precise targeted strategies. Second, we will delve into the mechanisms of macrophage recruitment and immune evasion driven by HPV infection and tumor hypoxia, supported by strong original experimental evidence. Finally, this review will critically evaluate the practical translational potential of various current therapeutic strategies targeting TAMs. It provides new perspectives for understanding the immune microenvironment of cervical cancer and lays the foundation for optimizing clinical treatment strategies and developing novel immune-targeted therapies.