Related Experiment Video
Updated: Jan 20, 2026
PI3K/mTOR/AKT Signaling Pathway
CD44 N-Glycosylation Alleviates Myocardial Ischemia-Reperfusion Through PI3K/AKT/mTOR Pathway
Yanxin Ren1,2, Haibin Dong2, Qingwen Huang2,3
1The 2nd Medical College of Binzhou Medical University, Yantai, Shandong, China.
Abstract:
Myocardial ischemia-reperfusion injury (MIRI) is one of the leading causes of morbidity and mortality from cardiovascular diseases worldwide. Protein N-glycosylation plays an important role in MIRI. However, there is limited knowledge regarding N-glycoproteins in MIRI and their alterations during MIRI. This study aims to investigate the dynamic changes of N-glycosylation modification in MIRI and the regulatory mechanisms of key proteins in MIRI to provide new therapeutic targets for the clinical diagnosis and treatment of MIRI. This study systematically explored the dynamic changes of N-glycosylation modification in MIRI through an integrated glycoproteomic analysis, combining a clinical sample, animal models, and cell models. Differential glycoproteins were identified using quantitative N-glycoproteomic mass spectrometry. Key regulatory molecules were screened through GO functional annotation and KEGG pathway enrichment. The integrated analysis identified 698 N-glycosylated proteins. Pathway enrichment analysis showed that the differentially expressed proteins were mainly involved in the PI3K/AKT/mTOR signaling pathway. The study of differentially expressed N-glycoproteins revealed that CD44 was upregulated and could regulate AKT. One possible reason is that N-glycosylation of CD44 affects its stability.
Insights
This study reveals dynamic N-glycosylation changes in myocardial ischemia-reperfusion injury (MIRI). Key protein CD44 was found to be upregulated, offering potential new therapeutic targets for MIRI treatment.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Proteomics
Background:
- Myocardial ischemia-reperfusion injury (MIRI) is a major cause of cardiovascular mortality.
- Protein N-glycosylation is implicated in MIRI, but its specific role and alterations remain poorly understood.
- Identifying N-glycoproteins in MIRI is crucial for developing new therapeutic strategies.
Purpose of the Study:
- To investigate dynamic N-glycosylation modifications in MIRI.
- To identify key N-glycoproteins and their regulatory mechanisms in MIRI.
- To provide novel therapeutic targets for MIRI diagnosis and treatment.
Main Methods:
- Integrated glycoproteomic analysis using clinical, animal, and cell models.
- Quantitative N-glycoproteomic mass spectrometry to identify differential glycoproteins.
- Gene Ontology (GO) functional annotation and KEGG pathway enrichment for regulatory molecule screening.
Main Results:
- Identified 698 N-glycosylated proteins in MIRI.
- Differentially expressed proteins are primarily involved in the PI3K/AKT/mTOR signaling pathway.
- Upregulation of CD44 was observed, with potential regulation of AKT, possibly due to N-glycosylation affecting CD44 stability.
Conclusions:
- Dynamic changes in N-glycosylation are significant in MIRI.
- The PI3K/AKT/mTOR pathway is a key player in MIRI-related N-glycosylation.
- CD44, modulated by N-glycosylation, presents a potential therapeutic target for MIRI.
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