Autophagy and multimodal programmed cell death and their crosstalk in ulcerative colitis
Li Zhang1, Dan Yang2, Helei Yu1
1Chengdu Pidu District Hospital of Traditional Chinese Medicine, Chengdu, Sichuan 610000, China.
Tissue & Cell
|June 2, 2026
Summary
This study explores how autophagy and programmed cell death (PCD) interact in ulcerative colitis (UC). Understanding these interactions may lead to new precision treatments for this chronic intestinal disease.
Area of Science:
- Gastroenterology
- Cell Biology
- Immunology
Background:
- Ulcerative colitis (UC) is a chronic intestinal inflammatory disease.
- Autophagy and programmed cell death (PCD) are increasingly recognized as key players in UC pathogenesis.
- The intricate interplay between autophagy and various PCD forms (ferroptosis, pyroptosis, necroptosis, cuproptosis, PANoptosis) in UC requires systematic elucidation.
Purpose of the Study:
- To systematically review the role of autophagy in UC.
- To detail the pathogenic involvement of multimodal PCD in UC.
- To elucidate the cross-regulatory mechanisms between autophagy and different PCD pathways in UC.
Main Methods:
- Systematic review of current literature on autophagy and PCD in UC.
- Analysis of the cross-regulation mechanisms between autophagy and ferroptosis, pyroptosis, necroptosis, cuproptosis, and PANoptosis.
- Evaluation of therapeutic strategies targeting the autophagy-PCD axis.
Main Results:
- Autophagy plays a core functional role in UC.
- Multimodal PCD pathways (ferroptosis, pyroptosis, necroptosis, cuproptosis, PANoptosis) contribute pathogenically to UC.
- Complex cross-regulatory networks exist between autophagy and these PCD pathways in the context of UC.
Conclusions:
- Targeting the autophagy-PCD interaction presents promising therapeutic strategies for UC.
- Further understanding of these pathways can inform personalized medicine approaches.
- Biomarker development and innovative delivery systems are crucial for translating these findings into clinical practice.
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