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NF-κB-dependent Signaling Pathway02:26

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Updated: May 28, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Research Progress on NINJ1-Mediated Plasma Membrane Rupture Regulation of Pathogen Infection Process.

Houjun Ran1,2, Xiaoquan Wang1,2, Kaituo Liu1,2

  • 1Joint International Research Laboratory of Agriculture and Agri-Product Safety, The Ministry of Education of China, Yangzhou University, Yangzhou 225009, China.

International Journal of Molecular Sciences
|May 27, 2026
PubMed
Summary
This summary is machine-generated.

Plasma membrane rupture (PMR) releases damage-associated molecular patterns (DAMPs), driving inflammation. New research reveals Nerve Injury-Induced Protein 1 (NINJ1) actively mediates PMR, offering therapeutic insights for various diseases.

Keywords:
NINJ1death pathogen infectiondisease treatmentlytic cellplasma membrane rupture (PMR)

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Area of Science:

  • Cell biology
  • Immunology
  • Pathology

Background:

  • Pathological events trigger plasma membrane rupture (PMR), releasing damage-associated molecular patterns (DAMPs).
  • DAMPs initiate inflammatory responses and can lead to cytokine storms, exacerbating tissue injury.
  • PMR was traditionally attributed to passive membrane pore formation, like pyroptosis or necroptosis.

Purpose of the Study:

  • To explore how diverse cell death pathways converge on PMR using pathogen infection as a model.
  • To detail the structure and function of Nerve Injury-Induced Protein 1 (NINJ1) as a key mediator of PMR.
  • To evaluate NINJ1-targeted therapies across infectious and non-infectious diseases involving PMR.

Main Methods:

  • Review of pathogen infection models to understand cell death pathway convergence on PMR.
  • Analysis of NINJ1's structure and function in mediating PMR.
  • Systematic evaluation of NINJ1-targeted therapeutic strategies in various disease contexts.

Main Results:

  • Multiple cell death pathways converge on PMR, particularly evident in pathogen infections.
  • Nerve Injury-Induced Protein 1 (NINJ1) is identified as a crucial executor of PMR through active oligomerization.
  • NINJ1 plays a significant role in PMR across both infectious and non-infectious inflammatory diseases.

Conclusions:

  • NINJ1 actively mediates PMR, challenging previous passive mechanisms.
  • Understanding NINJ1's role provides a unified perspective on PMR in diverse pathologies.
  • NINJ1-targeted strategies hold promise for treating a broad spectrum of PMR-driven diseases.