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However, whether this characterized phenomenon could account for periodontal pathogenesis under hyperglycemic conditions remains unclear. In this study, we assessed the senescent phenotypic changes in experimental periodontitis under hyperglycemic conditions. Next, we investigated the mitochondrial function and the potential mitophagy pathways in cellular senescence\n                    <jats:italic>in vitro<\/jats:italic>\n                    and\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Our findings showed that significant senescence occurred in the gingival tissues of diabetic periodontitis mice with increased expression of senescence\u2010related protein p21\n                    <jats:sup>Cip1<\/jats:sup>\n                    and the senescence\u2010associated secretory phenotype response as well as the decreased expression of NIP3\u2010like protein X (NIX), a mitochondrial receptor. Likewise, we showed that mitochondrial dysfunction (e.g., reduction of mitochondrial membrane potential and accumulation of reactive oxygen species) was attributed to cellular senescence in: human periodontal ligament cells (hPDLCs) through hyperglycemia\u2010induced and\n                    <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                    lipopolysaccharide (\n                    <jats:italic>P.g<\/jats:italic>\n                    \u2010LPS)\u2010induced oxidative stresses. Notably, the resulting reduced NIX expression was reversed by the use of the mitochondrial reactive oxygen species (ROS) scavenger N\u2010acetyl\u2010\n                    <jats:sc>l<\/jats:sc>\n                    \u2010cysteine (NAC), thus correcting the mitochondrial dysfunction. We further verified the expression of inflammatory mediators and senescence\u2010related factors in mice gingival tissues and identified the possible regulatory pathways. Taken together, our work demonstrates the critical role of cellular senescence and mitochondrial dysfunction in periodontal pathogenesis under hyperglycemic conditions. Hence, restoration of mitochondrial function may be a potential novel therapeutic approach to tackling periodontitis in diabetic patients.\n                  <\/jats:p>","DOI":"10.1111\/febs.17352","type":"journal-article","created":{"date-parts":[[2024,12,24]],"date-time":"2024-12-24T07:28:45Z","timestamp":1735025325000},"page":"1726-1742","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Attenuated\n                    <scp>NIX<\/scp>\n                    in impaired mitophagy contributes to exacerbating cellular senescence in experimental periodontitis under hyperglycemic conditions"],"prefix":"10.1111","volume":"292","author":[{"given":"Danni","family":"Song","sequence":"first","affiliation":[{"name":"Shanghai Engineering Research Center of Tooth Restoration and Regeneration &amp; Tongji Research Institute of Stomatology &amp; Department of Orthodontics, Stomatological Hospital and Dental School Tongji University  Shanghai China"},{"name":"Jiangxi Provincial Key Laboratory of Oral Diseases &amp; Jiangxi Provincial Clinical Research Center for Oral Diseases &amp; The Affiliated Stomatological Hospital, Jiangxi Medical College Nanchang University  Jiangxi China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beibei","family":"Chen","sequence":"additional","affiliation":[{"name":"Shanghai Engineering Research Center of Tooth Restoration and Regeneration &amp; Tongji Research Institute of Stomatology &amp; Department of Orthodontics, Stomatological Hospital and Dental School Tongji University  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianfan","family":"Cheng","sequence":"additional","affiliation":[{"name":"Division of Periodontology &amp; Implant Dentistry, Faculty of Dentistry The University of Hong Kong  Hong Kong 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