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<p>Efferocytosis, the process of apoptotic cell clearance, is a fundamental biological mechanism for maintaining tissue homeostasis. However, its role in disease pathogenesis is often oversimplified, neglecting a critical knowledge gap: how the single process could drive opposing pathological outcomes. This review provides a comprehensive analysis centered on the functional duality of efferocytosis. By synthesizing evidence across a spectrum of human pathologies—from atherosclerosis and neurodegeneration to cancer—we establish a core paradigm: impaired efferocytosis is a central pathogenic driver in chronic inflammatory and autoimmune diseases, leading to unresolved inflammation. Conversely, the hijacking of efferocytosis by tumors fosters an immunosuppressive microenvironment, facilitating immune evasion. This dichotomy presents a significant therapeutic conundrum, as enhancing efferocytosis benefits inflammatory conditions but exacerbates cancer. By dissecting these context-dependent mechanisms, we argue that the future of efferocytosis-based medicine hinges on developing targeted, disease-specific strategies to safely harness this powerful biological process.</p>

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Efferocytosis: the art of cellular clearance and novel perspectives in disease therapy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月23日

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  • Gege Li,
  • Jiashuai Xu,
  • Xiaohan Tian,
  • Jingyi Xiao,
  • Junqi Long,
  • Yining Chen,
  • Wenzhi Shen,
  • Shuangtao Zhao

摘要

Efferocytosis, the process of apoptotic cell clearance, is a fundamental biological mechanism for maintaining tissue homeostasis. However, its role in disease pathogenesis is often oversimplified, neglecting a critical knowledge gap: how the single process could drive opposing pathological outcomes. This review provides a comprehensive analysis centered on the functional duality of efferocytosis. By synthesizing evidence across a spectrum of human pathologies—from atherosclerosis and neurodegeneration to cancer—we establish a core paradigm: impaired efferocytosis is a central pathogenic driver in chronic inflammatory and autoimmune diseases, leading to unresolved inflammation. Conversely, the hijacking of efferocytosis by tumors fosters an immunosuppressive microenvironment, facilitating immune evasion. This dichotomy presents a significant therapeutic conundrum, as enhancing efferocytosis benefits inflammatory conditions but exacerbates cancer. By dissecting these context-dependent mechanisms, we argue that the future of efferocytosis-based medicine hinges on developing targeted, disease-specific strategies to safely harness this powerful biological process.