The Role of Mitochondrial Homeostasis in the Pathogenesis of Chronic Rhinosinusitis
5 affiliations
- 1ENT and Head and Neck Research Center and Department, School of Medicine, The Five Senses Health Institute Iran University of Medical Sciences Tehran Iran
- 2Department of Allergy and Clinical Immunology, Rasool‐e‐Akram Hospital Iran University of Medical Sciences Tehran Iran
- 3Skull Base Research Center, The Five Senses Health Institute, School of Medicine Iran University of Medical Sciences Tehran Iran
- 4Breast Cancer Research Center Iran University of Medical Sciences Tehran Iran
- 5Micro/Nano Technology Center Tokai University Hiratsuka‐shi Kanagawa Japan
Abstract
Background: Chronic rhinosinusitis (CRS) is a common clinical condition characterized by persistent inflammation of the nasal and sinus mucosa. While inflammatory endotypes are well‐described, the upstream metabolic dysregulations that initiate and perpetuate inflammation remain poorly defined. This review examines how mitochondrial metabolism, biogenesis, and dysfunction contribute to CRS pathogenesis.
Methods: A comprehensive literature search was performed up to November 2025 using PubMed/MEDLINE, Web of Science, and ScienceDirect. Search terms included “chronic rhinosinusitis,” “mitochondria,” “oxidative stress,” “reactive oxygen species,” “inflammation,” and “epithelial barrier,” together with related keywords and synonyms. Experimental, mechanistic, and translational studies exploring mitochondrial involvement in CRS were included.
Results: Evidence from multiple experimental studies demonstrates that mitochondrial dysfunction is closely intertwined with key pathological processes in CRS. Mitochondria are damaged by diverse CRS‐related pathogenic factors leading to excessive reactive oxygen species production, impaired biogenesis, and disrupted membrane potential. These mitochondrial abnormalities amplify epithelial inflammation, oxidative stress, and barrier dysfunction, creating a self‐propagating vicious cycle in which mitochondrial injury and inflammation reinforce each other. Mitochondrial dysfunction also contributes to characteristic histopathological changes, including epithelial damage, ciliary impairment, and fibrin deposition.
Conclusions: Mitochondria play a pivotal role in CRS pathogenesis. Targeting this self‐amplifying cycle of Inflammation–oxidative stress–mitochondrial dysfunction therefore represents a promising therapeutic strategy for breaking the chronicity of CRS.
Related
- Increased expression of hPGDS‑PGD2 in patients with eosinophilic chronic rhinosinusitis with nasal polyps
- Ocular Surface Findings in Patients with Surgery-Indicated Chronic Rhinosinusitis with Nasal Polyps: A Retrospective Study
- Endotype and Sample Site-Related Periostin Upregulation in Chronic Rhinosinusitis with Nasal Polyposis: A Systematic Review
- Interleukin-17 in the Nasal Polyps of Patients with Chronic Rhinosinusitis Compared to Healthy Controls: A Systematic Review
- Real‐World Treatment Escalation Patterns of Biologics and Functional Endoscopic Sinus Surgery in Chronic Rhinosinusitis (CRS): A Nationwide Database Study
BibTeX
@article{ghalehbaghi2026role,
title = {{The Role of Mitochondrial Homeostasis in the Pathogenesis of Chronic Rhinosinusitis}},
author = {Babak Ghalehbaghi and Morteza Fallahpour and Mohammad Nabavi and Maryam Jalessi and Hadi Ghanbari and Nasibeh Khayer and Farzad Taghizadeh‐Hesary},
journal = {Immunity, Inflammation and Disease},
year = {2026},
month = nov,
doi = {10.1002/iid3.70579},
url = {https://doi.org/10.1002/iid3.70579},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Role of Mitochondrial Homeostasis in the Pathogenesis of Chronic Rhinosinusitis
AU - Babak Ghalehbaghi
AU - Morteza Fallahpour
AU - Mohammad Nabavi
AU - Maryam Jalessi
AU - Hadi Ghanbari
AU - Nasibeh Khayer
AU - Farzad Taghizadeh‐Hesary
PY - 2026
DA - 2026/11/05
JO - Immunity, Inflammation and Disease
DO - 10.1002/iid3.70579
UR - https://doi.org/10.1002/iid3.70579
AB - Background: Chronic rhinosinusitis (CRS) is a common clinical condition characterized by persistent inflammation of the nasal and sinus mucosa. While inflammatory endotypes are well‐described, the upstream metabolic dysregulations that initiate and perpetuate inflammation remain poorly defined. This review examines how mitochondrial metabolism, biogenesis, and dysfunction contribute to CRS pathogenesis. Methods: A comprehensive literature search was performed up to November 2025 using PubMed/MEDLINE, Web of Science, and ScienceDirect. Search terms included “chronic rhinosinusitis,” “mitochondria,” “oxidative stress,” “reactive oxygen species,” “inflammation,” and “epithelial barrier,” together with related keywords and synonyms. Experimental, mechanistic, and translational studies exploring mitochondrial involvement in CRS were included. Results: Evidence from multiple experimental studies demonstrates that mitochondrial dysfunction is closely intertwined with key pathological processes in CRS. Mitochondria are damaged by diverse CRS‐related pathogenic factors leading to excessive reactive oxygen species production, impaired biogenesis, and disrupted membrane potential. These mitochondrial abnormalities amplify epithelial inflammation, oxidative stress, and barrier dysfunction, creating a self‐propagating vicious cycle in which mitochondrial injury and inflammation reinforce each other. Mitochondrial dysfunction also contributes to characteristic histopathological changes, including epithelial damage, ciliary impairment, and fibrin deposition. Conclusions: Mitochondria play a pivotal role in CRS pathogenesis. Targeting this self‐amplifying cycle of Inflammation–oxidative stress–mitochondrial dysfunction therefore represents a promising therapeutic strategy for breaking the chronicity of CRS.
SN - 2050-4527
ER -