Ruptosis: a novel hormone-triggered cytotoxic cell death program linking endocrine homeostasis to innate immunity
Feng Tang1,2
1Brain Glioma Center, Department of Neurosurgery, Zhongnan Hospital of Wuhan University, Wuhan, 430061, Hubei, China. tf172126@163.com.
None:
A landmark 2026 Cell publication by Chai et al. characterized Ruptosis, a previously unclassified form of regulated cell death executed by specialized glandular immune cells termed ruptoblasts in the planarian Schmidtea mediterranea. Triggered exclusively by elevated activin (a dual hormone/inflammatory cytokine), Ruptosis manifests rapid, contact-independent explosive cellular disintegration and releases diffusible toxins to eliminate aberrant somatic cells, stem cells and invading bacteria. Distinct from apoptosis, pyroptosis, necroptosis, ferroptosis and neutrophil NETosis at morphological, biochemical and kinetic levels, this novel lytic pathway substantially expands the canonical regulated cell death (RCD) classification system. This commentary outlines the defining unique features of Ruptosis and discusses its evolutionary implications for cell death and innate immunity research.
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