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July 29, 2026Cellular and Molecular Life SciencesOpen Access

NLRC3 deficiency exacerbates high-fat diet-induced enteric nervous system injury and colonic motility dysfunction in mice via activating NF-κB signaling pathway

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Authors

YWYue WangYLY P LiYLY P Li

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Overview

Randomized trial shows NLRC3 deficiency increases enteric nervous system injury in mice, indicating its potential as a therapeutic target.

Key Points

  • Investigate the role of NLRC3 in the enteric nervous system and its impact on high-fat diet-induced injury.
  • Established HFD-induced colonic inflammation model in Nlrc3 −/− and WT mice.
  • Assessed NLRC3 expression and distribution in the ENS with morphological and molecular assays.
  • Evaluated colonic motility function in response to NLRC3 deficiency.
  • HFD decreased NLRC3 expression in enteric neurons, correlating with increased ENS injury in Nlrc3 −/− mice.
  • Nlrc3 −/− mice exhibited more severe neuronal loss and structural disruption compared to WT after HFD.
  • Activation of NF-κB signaling pathway was linked to increased neuronal apoptosis in NLRC3 deficient models.

Cite This Study

Wang et al. (2026) studied this question.

synapsesocial.com/papers/6a69a2fcc8da07d9defa720dhttps://doi.org/10.1007/s00018-026-06364-1
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