Published online Dec 28, 2023. doi: 10.3748/wjg.v29.i48.6222
Peer-review started: September 22, 2023
First decision: November 20, 2023
Revised: November 27, 2023
Accepted: December 14, 2023
Article in press: December 14, 2023
Published online: December 28, 2023
Processing time: 95 Days and 16.4 Hours
Ulcerative colitis (UC) is a chronic gastrointestinal disorder characterized by inflammation and ulceration, representing a significant predisposition to colorectal cancer. Recent advances in single-cell RNA sequencing (scRNA-seq) technology offer a promising avenue for dissecting the complex cellular inter-actions and molecular signatures driving UC pathology.
To utilize scRNA-seq technology to dissect the complex cellular interactions and molecular signatures that underlie UC pathology.
In this research, we integrated and analyzed the scRNA-seq data from UC patients. Moreover, we conducted mRNA and protein level assays as well as pathology-related staining tests on clinical patient samples.
In this study, we identified the sustained upregulation of inflammatory response pathways during UC progression, characterized the features of damaged endo-thelial cells in colitis. Furthermore, we uncovered the downregulation of phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) has a negative correlation with signal transducer and activator of transcription 3. Significant downregulation of LHPP in UC patient tissues and plasma suggests that LHPP may serve as a potential therapeutic target for UC. This paper highlights the importance of LHPP as a potential key target in UC and unveils its potential role in inflammation regulation.
The findings suggest that LHPP may serve as a potential therapeutic target for UC, emphasizing its importance as a potential key target in UC and unveiling its role in inflammation regulation.
Core Tip: Ulcerative colitis (UC), a chronic inflammatory bowel disease linked to colorectal cancer, was investigated using single-cell RNA sequencing technology. The study unveiled sustained upregulation of inflammatory response pathways and characterized damaged endothelial cells during UC progression. Notably, the downregulation of phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP) exhibited a negative correlation with signal transducer and activator of transcription 3. LHPP's significant downregulation in UC patient tissues and plasma suggests its potential as a therapeutic target. The findings highlight LHPP as a key target in UC and emphasize its role in inflammation regulation, offering insights for potential therapeutic interventions.