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In order to explore the spectrum of mitochondrial DNA (mtDNA) mutations in Korean patients with Leber's hereditary optic neuropathy (LHON), we investigated the spectrum of mtDNA mutations in 145 Korean probands confirmed with the diagnosis of LHON. Total genomic DNA was isolated from the peripheral blood leukocytes of the patients with suspected LHON, and mtDNA mutations were identified by direct sequencing. Analysis of mtDNA mutations revealed seven primary LHON mutations including the nucleotide positions (nps) 11778A (101 probands, 69.2%), 14484C (31 probands, 21.2%), 3460A (5 probands, 3.4%), and G3635A, G3733A, C4171A, and G13051A mutations in one proband each. In addition, two provisional mtDNA mutations at nps T3472C, and G13259A were each found in one proband, respectively. Another provisional mtDNA mutation at np T3394C was found in two probands. In conclusion, the spectrum of mtDNA mutations in Korean patients with LHON may differ from other ethnicities, which is characterized by high prevalence of 11778A and 14484C mutations, and a low prevalence of the 3460A mutation.
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http://dx.doi.org/10.1038/s41598-024-56215-x | DOI Listing |
J Affect Disord
September 2025
Department of Psychiatry, The Affiliated Kangning Hospital of Ningbo University, Ningbo Kangning Hospital, Ningbo, China; Medical Center, Ningbo University, Ningbo, China. Electronic address:
Objective: This study aimed to identify potential mutations associated with major depressive disorder (MDD) and evaluate disease-associated risk factors.
Methods: Total genomic DNAwas extracted from the participants' blood samples, and the complete mitochondrial genome wasamplified by PCR, purified, and sequenced. Mutation burden analysis and functional mutation analysis was performed, including total mutation counts, highly conserved mutations (Conservation Index >75 %), and structurally disruptive mutations.
Cell Rep
September 2025
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address:
Purifying selection that limits the transmission of harmful mitochondrial DNA (mtDNA) mutations has been observed in both human and animal models. Yet, the precise mechanism underlying this process remains undefined. Here, we present a highly specific and efficient in situ imaging method capable of visualizing mtDNA variants that differ by only a few nucleotides at single-molecule resolution in Drosophila ovaries.
View Article and Find Full Text PDFCurr Med Chem
August 2025
Laboratory of Molecular Genetic Modeling of Inflammaging, Institute of General Pathology and Pathophysiology, 8, Baltiiskaya Street, 125315 Moscow, Russia.
Science
September 2025
Division of Nephrology and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Somatically acquired mitochondrial DNA mutations accumulate with age, but the mechanisms and consequences are poorly understood. Here we show that transient injuries induce a burst of persistent mtDNA mutations that impair resilience to future injuries. mtDNA mutations suppressed energy-intensive nucleotide metabolism.
View Article and Find Full Text PDFAnn Med Surg (Lond)
September 2025
University of Debrecen, Debrecen, Hungary.
Myeloproliferative neoplasms (MPNs) are clonal disorders of hematopoietic stem cells characterized by aberrant proliferation of myeloid lineages, driven primarily by mutations in JAK2, CALR, and myeloproliferative leukemia, leading to constitutive activation of the JAK-STAT pathway. Emerging evidence highlights mitochondrial dysfunction as a key factor in MPN pathogenesis, contributing to increased reactive oxygen species production, mitochondrial DNA mutations, and dysregulated mitochondrial dynamics, which collectively promote clonal expansion and apoptosis resistance. Targeting mitochondrial pathways has gained attention as a therapeutic strategy, with approaches including mitochondria-targeted antioxidants, metabolic inhibitors, and modulation of mitophagy and mitochondrial fission/fusion dynamics.
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