DOI QR코드

DOI QR Code

The role of endoplasmic reticulum stress in the pathogenesis of oral diseases

  • Kezia Rachellea Mustakim (Department of Oral and Maxillofacial Surgery, Dental Research Institute, School of Dentistry, Seoul National University) ;
  • Mi Young Eo (Department of Oral and Maxillofacial Surgery, Dental Research Institute, School of Dentistry, Seoul National University) ;
  • Soung Min Kim (Department of Oral and Maxillofacial Surgery, Dental Research Institute, School of Dentistry, Seoul National University)
  • 투고 : 2023.08.20
  • 심사 : 2023.10.13
  • 발행 : 2024.08.31

초록

The endoplasmic reticulum (ER) is crucial for protein synthesis, transport, and folding, as well as calcium storage, lipid and steroid synthesis, and carbohydrate metabolism. Endoplasmic reticulum stress (ERS) occurs when misfolded or unfolded proteins accumulate in the ER lumen due to increased protein secretion or impaired folding. While the role of ERS in disease pathogenesis has been widely studied, most research has focused on extraoral diseases, leaving the role of ERS in intraoral diseases unclear. This review examines the role of ERS in oral diseases and oral fibrosis pathogenesis. A systematic search of literature through July 2023 was conducted in the MEDLINE database (via PubMed) using specific terms related to ERS, oral diseases, and fibrosis. The findings were summarized in both table and narrative form. Emerging evidence indicates that ERS significantly contributes to the pathogenesis of oral diseases and fibrosis. ERS-induced dysregulation of protein folding and the unfolded protein response can lead to cellular dysfunction and inflammation in oral tissues. Understanding the relationship between ERS and oral disease pathogenesis could offer new therapeutic targets for managing oral health and fibrosis-related complications.

키워드

과제정보

This study was supported by the National Research Foundation of Korea through the Ministry of Education (2022R1I1A1A01070644) and by the Ministry of Science and ICT (2022R1F1A1069624).

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