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 intestinal condition characterized by inflammation and ulceration, and it is a significant risk factor for 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.
A comprehensive understanding of the cellular and molecular mechanisms underlying UC development and progression remains elusive, and there is a growing need for more precise and targeted therapeutic interventions.
The object of this study is to utilize scRNA-seq technology to dissect the complex cellular interactions and molecular signatures that underlie UC pathology.
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.
We identified the sustained upregulation of inflammatory response pathways during UC progression, characterized the features of damaged endothelial 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.
This study suggests 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.
This study sheds light on the cellular and molecular mechanisms driving UC pathogenesis. These insights provide a foundation for future research into potential therapeutic interventions, with LHPP emerging as a key player in UC regulation and the immune response. Ultimately, unraveling the complexities of UC at the single-cell level holds promise for more effective treatments and improved outcomes for patients with this challenging condition.