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<p>Caspase-1, a cysteinyl aspartate-specific protease central to inflammasome activation, acts as a master regulator of multiple programmed cell death (PCD) pathways including pyroptosis, apoptosis, necroptosis, ferroptosis, and PANoptosis. It interacts with other caspases and is tightly modulated by epigenetic mechanisms and post-translational modifications. During the tumor microenvironment and immune metabolic regulation, it is activated and acts in a context-dependent way. Given this multifaceted involvement in cancer, neurodegenerative diseases and autoimmune disorders, caspase-1 represents a promising yet challenging therapeutic target. Despite extensive research, challenges persist in the insufficient understanding of crossover mechanisms and research of caspase-1 inhibitors. This review systematically clarifies its paradoxical roles by integrating caspase-1’ s regulatory and context-dependent networks across PCD, epigenetics, tumor microenvironment, immune metabolism, and diverse diseases. Additionally, we summarize therapeutic progress and root causes of caspase-1 inhibitors’ clinical failure as well as putting forward some innovative treatment strategies, aiming to offer new perspectives for future treating design.</p>

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Caspase-1 in cancer and inflammatory diseases: a potential therapeutic target

  • 期刊论文

  • 发表日期：

    2026年3月5日

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  • Xuan Sun,
  • Wen-Bin Ou

摘要

Caspase-1, a cysteinyl aspartate-specific protease central to inflammasome activation, acts as a master regulator of multiple programmed cell death (PCD) pathways including pyroptosis, apoptosis, necroptosis, ferroptosis, and PANoptosis. It interacts with other caspases and is tightly modulated by epigenetic mechanisms and post-translational modifications. During the tumor microenvironment and immune metabolic regulation, it is activated and acts in a context-dependent way. Given this multifaceted involvement in cancer, neurodegenerative diseases and autoimmune disorders, caspase-1 represents a promising yet challenging therapeutic target. Despite extensive research, challenges persist in the insufficient understanding of crossover mechanisms and research of caspase-1 inhibitors. This review systematically clarifies its paradoxical roles by integrating caspase-1’ s regulatory and context-dependent networks across PCD, epigenetics, tumor microenvironment, immune metabolism, and diverse diseases. Additionally, we summarize therapeutic progress and root causes of caspase-1 inhibitors’ clinical failure as well as putting forward some innovative treatment strategies, aiming to offer new perspectives for future treating design.