Objective: Since mitochondrial DNA (mtDNA) mutations have been established to associate with the aging process and some degenerative diseases, we investigated the correlation between idiopathic osteoarthritis (OA) and the 4977-bp mtDNA deletion.
Design: Cartilage were collected from six sites in knee joints removed from 18 aged patients with idiopathic OA, 10 aged non-OA cadavers, 3 young cadavers (YC), and lateral femoral condyle of 9 young patients. Histopathologic changes were examined and the common 4977-bp mtDNA deletions were analyzed in young and elderly cartilages obtained from different sites in the knee joint. The association of the 4977-bp deletion of mtDNA with idiopathic OA and aging was evaluated.
Results: The 4977-bp mtDNA deletion was detected in 17 of the 18 OA patients, 9 of the 10 aged non-OA cadavers, and 1 of the 3 YC. None of the nine specimens collected from the lateral femoral condyle of young patients had a detectable deletion of mtDNA. The 4977-bp mtDNA deletion was not significantly correlated with the severity of OA graded by the Mankin score. The frequencies of occurrence of the 4977-bp mtDNA deletion were significantly different between the OA group and the aged non-OA control group (P=0.004) and between the aged non-OA group and the young control group (P=0.002).
Conclusions: The results suggest that accumulation of the 4977-bp deletion of mtDNA in knee cartilage increases with age and may play a role in the development of idiopathic OA in the knee joint.
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http://dx.doi.org/10.1016/j.joca.2005.06.011 | DOI Listing |
Neuropathol Appl Neurobiol
February 2025
Department of Neurology, Shandong Key Laboratory of Mitochondrial Medicine and Rare Diseases, Research Institute of Neuromuscular and Neurodegenerative Diseases, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Background: Progressive external ophthalmoplegia (PEO) is a classic manifestation of mitochondrial disease. However, the link between its genetic characteristics and clinical presentations remains poorly investigated.
Methods: We analysed the clinical, pathological and genetic characteristics of a large cohort of patients with PEO, based on the type of their mtDNA variations.
J Am Acad Dermatol
November 2024
Department of Dermatology, George Washington University, School of Medicine and Health Sciences, Washington, District of Columbia. Electronic address:
Background: UV-A radiation contributes to photoaging/photocarcinogenesis by generating inflammation and oxidative damage. Current photoprotective strategies are limited by the availability/utilization of UV-A filters, highlighting an unmet need. Cannabidiol (CBD), having anti-inflammatory/antioxidant properties via regulation of nuclear erythroid 2-related factor, heme oxygenase 1, and peroxisome proliferator-activated receptor gamma, could potentially mitigate damage from UV-A exposure.
View Article and Find Full Text PDFAndrology
March 2024
Institute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, Hunan, China.
Andrologia
November 2022
Department of Biology & Anatomical Sciences, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Semen parameters have been found to predict reproductive success poorly and are the most prevalent diagnostic tool for male infertility. There are few conflicting reports regarding the correlation of DNMT genes expression, mitochondrial DNA copy number (mtDNAcn) and deletion (mtDNAdel) with different sperm parameters. To investigate DNMT mRNA level, mtDNAcn and deletion in infertile men, with different sperm parameters, compared with fertile men, semen samples from 30 men with unknown male infertility and normal sperm parameters (experimental group I), 30 infertile patients with at least two abnormal sperm parameters (experimental group II) and 30 fertile normozoospermic men (control group) were collected.
View Article and Find Full Text PDFJ Neurovirol
April 2022
Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA, 92093, USA.
Human immunodeficiency virus (HIV) infection is potentially associated with premature aging, but demonstrating this is difficult due to a lack of reliable biomarkers. The mitochondrial (mt) DNA "common deletion" mutation (mtCDM) is a 4977-bp deletion associated with aging and neurodegenerative diseases. We examined how mtDNA and mtCDM correlate with markers of neurodegeneration and inflammation in people with and without HIV (PWH and PWOH).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!