{"title":"Glycolysis Plays a Critical and Dual Role in Periodontitis","authors":"Hongyu Ming, Yingyao Li, Tongyun Chen, Xinze Wu, Xudong Xie","doi":"10.1002/jcp.70098","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Glycolysis is a fundamental metabolic pathway that breaks down glucose into pyruvate and lactate, critically shaping immune responses and cell functions in various diseases. Periodontitis is a chronic inflammatory disease marked by progressive destruction of periodontal tissues. Recent evidence has revealed that glycolysis plays a critical and dual role in periodontitis. On one hand, metabolic reprogramming toward glycolysis amplifies inflammatory cascades in various periodontal cells, driving periodontitis progression through multiple mechanisms. On the other hand, the end-product of glycolysis, lactate, and its lactylation exert anti-inflammatory effects in periodontitis by modulating immune responses and regulating bone remodeling. Moreover, emerging therapeutic strategies targeting glycolytic flux aim to inhibit periodontal inflammation progression and promote periodontal tissue regeneration. In this review, we illustrate the dual mechanisms of glycolysis in periodontitis pathogenesis and highlight its potential as a therapeutic target for metabolic intervention.</p>\n </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 9","pages":""},"PeriodicalIF":4.0000,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cellular Physiology","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jcp.70098","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Glycolysis is a fundamental metabolic pathway that breaks down glucose into pyruvate and lactate, critically shaping immune responses and cell functions in various diseases. Periodontitis is a chronic inflammatory disease marked by progressive destruction of periodontal tissues. Recent evidence has revealed that glycolysis plays a critical and dual role in periodontitis. On one hand, metabolic reprogramming toward glycolysis amplifies inflammatory cascades in various periodontal cells, driving periodontitis progression through multiple mechanisms. On the other hand, the end-product of glycolysis, lactate, and its lactylation exert anti-inflammatory effects in periodontitis by modulating immune responses and regulating bone remodeling. Moreover, emerging therapeutic strategies targeting glycolytic flux aim to inhibit periodontal inflammation progression and promote periodontal tissue regeneration. In this review, we illustrate the dual mechanisms of glycolysis in periodontitis pathogenesis and highlight its potential as a therapeutic target for metabolic intervention.
期刊介绍：
The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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