{"title":"线粒体自噬及其在牙周病中的意义。","authors":"Guliqihere Abulaiti, Xu Qin, Lili Chen, Guangxun Zhu","doi":"10.1111/odi.15279","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Periodontal disease is a common chronic inflammatory condition affecting the tissues that support teeth, leading to their destruction. Mitophagy, a specialized form of autophagy responsible for degrading damaged mitochondria, plays a crucial role in maintaining cellular homeostasis. However, its role in periodontal disease progression remains poorly understood. This review aims to summarize recent research on mitophagy's role in periodontal disease pathogenesis.</p><p><strong>Methods: </strong>A comprehensive literature review on mitophagy was conducted using PubMed, Scopus, and Web of Science databases, employing keywords related to periodontal disease such as \"periodontal,\" \"periodontitis,\" \"gingiva,\" and \"gingivitis.\"</p><p><strong>Results: </strong>A review of 18 original studies revealed that mitophagy plays a crucial role in periodontal disease by regulating key pathophysiological mechanisms. Specifically, mitophagy modulates periodontal inflammation by influencing pro-inflammatory cytokines and mitochondrial reactive oxygen species. Additionally, it is essential for alveolar bone remodeling, impacting both bone resorption and regeneration. Mitophagy also regulates cell apoptosis within periodontal tissues, helping to preserve cellular function and tissue integrity during periodontal disease progression.</p><p><strong>Conclusions: </strong>Mitophagy regulates periodontal disease pathogenesis by modulating inflammation, bone remodeling, and cell death in periodontal tissues. Further research is needed to explore its therapeutic potential in periodontal disease treatment and improve targeted interventions.</p>","PeriodicalId":19615,"journal":{"name":"Oral diseases","volume":" ","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Mitophagy and Its Significance in Periodontal Disease.\",\"authors\":\"Guliqihere Abulaiti, Xu Qin, Lili Chen, Guangxun Zhu\",\"doi\":\"10.1111/odi.15279\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>Periodontal disease is a common chronic inflammatory condition affecting the tissues that support teeth, leading to their destruction. Mitophagy, a specialized form of autophagy responsible for degrading damaged mitochondria, plays a crucial role in maintaining cellular homeostasis. However, its role in periodontal disease progression remains poorly understood. This review aims to summarize recent research on mitophagy's role in periodontal disease pathogenesis.</p><p><strong>Methods: </strong>A comprehensive literature review on mitophagy was conducted using PubMed, Scopus, and Web of Science databases, employing keywords related to periodontal disease such as \\\"periodontal,\\\" \\\"periodontitis,\\\" \\\"gingiva,\\\" and \\\"gingivitis.\\\"</p><p><strong>Results: </strong>A review of 18 original studies revealed that mitophagy plays a crucial role in periodontal disease by regulating key pathophysiological mechanisms. Specifically, mitophagy modulates periodontal inflammation by influencing pro-inflammatory cytokines and mitochondrial reactive oxygen species. Additionally, it is essential for alveolar bone remodeling, impacting both bone resorption and regeneration. Mitophagy also regulates cell apoptosis within periodontal tissues, helping to preserve cellular function and tissue integrity during periodontal disease progression.</p><p><strong>Conclusions: </strong>Mitophagy regulates periodontal disease pathogenesis by modulating inflammation, bone remodeling, and cell death in periodontal tissues. Further research is needed to explore its therapeutic potential in periodontal disease treatment and improve targeted interventions.</p>\",\"PeriodicalId\":19615,\"journal\":{\"name\":\"Oral diseases\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-02-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oral diseases\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/odi.15279\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"DENTISTRY, ORAL SURGERY & MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral diseases","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/odi.15279","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
引用次数: 0
摘要
目的：牙周病是一种常见的慢性炎症，影响支撑牙齿的组织，导致牙齿的破坏。线粒体自噬是一种特殊形式的自噬，负责降解受损的线粒体，在维持细胞稳态中起着至关重要的作用。然而，它在牙周病进展中的作用仍然知之甚少。本文综述了近年来有关线粒体自噬在牙周病发病机制中的作用的研究进展。方法：利用PubMed、Scopus、Web of Science等数据库，采用“牙周”、“牙周炎”、“牙龈”、“牙龈炎”等牙周病相关关键词，对有关线粒体自噬的文献进行综述。“结果：对18项原始研究的回顾表明，有丝分裂通过调节关键的病理生理机制在牙周病中起着至关重要的作用。具体来说，线粒体自噬通过影响促炎细胞因子和线粒体活性氧来调节牙周炎症。此外，它对牙槽骨重塑至关重要，影响骨吸收和再生。线粒体自噬也调节牙周组织内的细胞凋亡，有助于在牙周病进展过程中保持细胞功能和组织完整性。结论：有丝分裂通过调节牙周组织的炎症、骨重塑和细胞死亡来调节牙周病的发病机制。需要进一步研究其在牙周病治疗中的潜力，并改进有针对性的干预措施。
Mitophagy and Its Significance in Periodontal Disease.
Objectives: Periodontal disease is a common chronic inflammatory condition affecting the tissues that support teeth, leading to their destruction. Mitophagy, a specialized form of autophagy responsible for degrading damaged mitochondria, plays a crucial role in maintaining cellular homeostasis. However, its role in periodontal disease progression remains poorly understood. This review aims to summarize recent research on mitophagy's role in periodontal disease pathogenesis.
Methods: A comprehensive literature review on mitophagy was conducted using PubMed, Scopus, and Web of Science databases, employing keywords related to periodontal disease such as "periodontal," "periodontitis," "gingiva," and "gingivitis."
Results: A review of 18 original studies revealed that mitophagy plays a crucial role in periodontal disease by regulating key pathophysiological mechanisms. Specifically, mitophagy modulates periodontal inflammation by influencing pro-inflammatory cytokines and mitochondrial reactive oxygen species. Additionally, it is essential for alveolar bone remodeling, impacting both bone resorption and regeneration. Mitophagy also regulates cell apoptosis within periodontal tissues, helping to preserve cellular function and tissue integrity during periodontal disease progression.
Conclusions: Mitophagy regulates periodontal disease pathogenesis by modulating inflammation, bone remodeling, and cell death in periodontal tissues. Further research is needed to explore its therapeutic potential in periodontal disease treatment and improve targeted interventions.
期刊介绍：
Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.
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