Gong ZZ, Li T, Yan H, Xu MH, Lian Y, Yang YX, Wei W, Liu T. Exploring the autophagy-related pathogenesis of active ulcerative colitis. World J Clin Cases 2024; 12(9): 1622-1633 [PMID: 38576744 DOI: 10.12998/wjcc.v12.i9.1622]
Corresponding Author of This Article
Tao Liu, PhD, Associate Professor, Chief Doctor, Wangjing Hospital, China Academy of Chinese Medical Sciences, Huajiadi Street, Chaoyang District, Beijing 100102, China. ltlyf2@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Clinical and Translational Research
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Cases. Mar 26, 2024; 12(9): 1622-1633 Published online Mar 26, 2024. doi: 10.12998/wjcc.v12.i9.1622
Exploring the autophagy-related pathogenesis of active ulcerative colitis
Zhuo-Zhi Gong, Teng Li, He Yan, Min-Hao Xu, Yue Lian, Yi-Xuan Yang, Wei Wei, Tao Liu
Zhuo-Zhi Gong, Teng Li, He Yan, Yue Lian, Wei Wei, Tao Liu, Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing 100102, China
Min-Hao Xu, College of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Beijing 100102, China
Yi-Xuan Yang, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China
Author contributions: Gong ZZ and Li T designed and supervised this study, wrote the manuscript; Yan H collated the data; Xu MH and Lian Y analyzed the data; Wei W and Liu T supervised this study and guided the revision of the article; all authors approved the final version of the article.
Institutional review board statement: The data of this study are publicly available on the GEO database, Human Autophagy database.
Conflict-of-interest statement: The authors declare no competing interests.
Data sharing statement: The data of this study are publicly available on the GEO database, Human Autophagy database.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Tao Liu, PhD, Associate Professor, Chief Doctor, Wangjing Hospital, China Academy of Chinese Medical Sciences, Huajiadi Street, Chaoyang District, Beijing 100102, China. ltlyf2@163.com
Received: January 7, 2024 Peer-review started: January 7, 2024 First decision: January 16, 2024 Revised: January 23, 2024 Accepted: February 27, 2024 Article in press: February 27, 2024 Published online: March 26, 2024
Abstract
BACKGROUND
The pathogenesis of ulcerative colitis (UC) is complex, and recent therapeutic advances remain unable to fully alleviate the condition.
AIM
To inform the development of novel UC treatments, bioinformatics was used to explore the autophagy-related pathogenesis associated with the active phase of UC.
METHODS
The GEO database was searched for UC-related datasets that included healthy controls who met the screening criteria. Differential analysis was conducted to obtain differentially expressed genes (DEGs). Autophagy-related targets were collected and intersected with the DEGs to identiy differentially expressed autophagy-related genes (DEARGs) associated with active UC. DEARGs were then subjected to KEGG, GO, and DisGeNET disease enrichment analyses using R software. Differential analysis of immune infiltrating cells was performed using the CiberSort algorithm. The least absolute shrinkage and selection operator algorithm and protein-protein interaction network were used to narrow down the DEARGs, and the top five targets in the Dgree ranking were designated as core targets.
RESULTS
A total of 4822 DEGs were obtained, of which 58 were classified as DEARGs. SERPINA1, BAG3, HSPA5, CASP1, and CX3CL1 were identified as core targets. GO enrichment analysis revealed that DEARGs were primarily enriched in processes related to autophagy regulation and macroautophagy. KEGG enrichment analysis showed that DEARGs were predominantly associated with NOD-like receptor signaling and other signaling pathways. Disease enrichment analysis indicated that DEARGs were significantly linked to diseases such as malignant glioma and middle cerebral artery occlusion. Immune infiltration analysis demonstrated a higher presence of immune cells like activated memory CD4 T cells and follicular helper T cells in active UC patients than in healthy controls.
CONCLUSION
Autophagy is closely related to the active phase of UC and the potential targets obtained from the analysis in this study may provide new insight into the treatment of active UC patients.
Core Tip: This study used bioinformatics to explore the autophagy-related pathogenesis of ulcerative colitis (UC) during its active phase. A total of 58 differentially expressed autophagy-related genes (DEARGs) were found in gene expression datasets from UC patients and healthy controls. Of these, SERPINA1, BAG3, HSPA5, CASP1, and CX3CL1 were identified as core targets. Enrichment analysis highlighted the involvement of DEARGs in autophagy regulation, and macroautophagy, in addition to NOD-like receptor signaling and other pathways. These DEARGs were also shown to be associated with diseases like malignant glioma and middle cerebral artery occlusion. Immune infiltration analysis revealed an increased presence of immune cells, including activated memory CD4 T cells and follicular helper T cells in active UC patients than in healthy controls. This study suggests that autophagy plays a significant role in the active phase of UC and identifies potential targets for novel UC treatments.
