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Interplay between metabolic reprogramming and post-translational modifications: from glycolysis to lactylation
Hengwei Wu1,2,3,4, He Huang1,2,3,4, Yanmin Zhao1,2,3,4
1Bone Marrow Transplantation Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
T cell activation involves metabolic reprogramming, shifting from oxidative phosphorylation to glycolysis. Glycolysis byproduct lactate modifies histones, impacting gene expression through lactylation, a key epigenetic regulator.
Area of Science:
- Immunology
- Cellular Metabolism
- Epigenetics
Background:
- Cellular metabolism dictates cell fate and function.
- Quiescent T cells rely on oxidative phosphorylation (OXPHOS) for survival.
- Antigen activation triggers rapid T cell metabolic reprogramming, favoring glycolysis for proliferation.
Purpose of the Study:
- To review T cell metabolic reprogramming and its impact on immune function.
- To explore the role of lactate and lactylation in cellular regulation.
- To elucidate the intersection of metabolic reprogramming and epigenetics.
Main Methods:
- Literature review of studies on T cell metabolism, lactate, and epigenetics.
- Analysis of metabolic pathways (glycolysis, OXPHOS) in T cells.
- Examination of histone lactylation as a regulatory mechanism.
Main Results:
- T cell activation significantly shifts metabolism towards glycolysis.
- Lactate, a glycolysis byproduct, directly modifies histones (lactylation).
- Lactylation influences gene transcription and cellular functions.
Conclusions:
- Metabolic reprogramming is crucial for T cell activation and function.
- Lactate-mediated lactylation represents a novel epigenetic regulatory pathway.
- Understanding these metabolic and epigenetic interactions is vital for immune regulation and disease.
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