The clinical presentation of mitochondrial DNA (mtDNA) disorders is quite diverse. Very often, the initial symptoms do not fit a specific disease, and diagnosis is difficult to make. We describe a patient who presented with macrocytic anemia. Extensive biochemical and clinical work-up failed to provide an etiology for the macrocytic anemia. The patient over the course of 6 years developed gait problems, exercise intolerance, episodic vomiting, short stature, dermatological problems, and recurrent infection. At age 8 years she had encephalopathy with ataxia and dysphagia. The presence of elevated lactate, bilateral basal ganglia calcification, and ragged red fibers led to mtDNA mutational analysis. A novel 4.4-kb deletion from nucleotide position 10,560 to nucleotide position 14, 980 was identified in muscle biopsy. The same heteroplasmic mtDNA deletion was present in blood, buccal cells, and hair follicles, but not in mother's blood, consistent with sporadic mutation in the patient. This case emphasizes the importance of considering mtDNA disorder in patients with multisystemic symptoms that cannot be explained by a specific diagnosis.
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Front Public Health
January 2025
School of Public Health, Gansu University of Chinese Medicine, Lanzhou, China.
Objective: To investigate the role of PCBP1 in the inhibition of lung adenocarcinoma proliferation by carbon irradiation.
Methods: A549 cells were irradiated with different doses of carbon ions to observe clonal survival and detect changes in cell proliferation. Whole transcriptome sequencing and the Illumina platform were used to analyze the differentially expressed genes in A549 cells after carbon ion irradiation.
Biol Psychiatry Glob Open Sci
March 2025
Initiative on Stress, Trauma, and Resilience, Department of Psychiatry and Human Behavior, Warren Alpert Medical School, Brown University, Providence, Rhode Island.
Background: Mounting evidence suggests that mitochondria respond to psychosocial stress. Recent studies suggest mitochondrial DNA (mtDNA) deletions may be increased in some psychiatric disorders, but no studies have examined early-life stress (ELS) and mtDNA deletions. In this study, we assessed mtDNA deletions in peripheral blood mononuclear cells of medically healthy young adults with and without ELS.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Neurology, Center for Medical Research on Innovation and Translation, Institute of Clinical Medicine, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Abnormality in transactivating response region DNA binding protein 43 (TDP43) is well-recognized as the pathological hallmark of neurodegenerative diseases. However, the role of TDP43 in neuromyelitis optica spectrum disorder (NMOSD) remains unknown. Here, our observations demonstrate an upregulation of TDP43 in both in vitro and in vivo models of NMOSD, as well as in biological samples from NMOSD patients.
View Article and Find Full Text PDFSci China Life Sci
January 2025
Institute of Rare Diseases, West China Hospital of Sichuan University, Sichuan University, Chengdu, 610000, China.
Human mitochondrial DNA (mtDNA) harbors essential mutations linked to aging, neurodegenerative diseases, and complex muscle disorders. Due to its uniparental and haploid inheritance, mtDNA captures matrilineal evolutionary trajectories, playing a crucial role in population and medical genetics. However, critical questions about the genomic diversity patterns, inheritance models, and evolutionary and medical functions of mtDNA remain unresolved or underexplored, particularly in the transition from traditional genotyping to large-scale genomic analyses.
View Article and Find Full Text PDFNature
January 2025
Changping Laboratory, Beijing, The People's Republic of China.
The development of animal models is crucial for studying and treating mitochondrial diseases. Here we optimized adenine and cytosine deaminases to reduce off-target effects on the transcriptome and the mitochondrial genome, improving the accuracy and efficiency of our newly developed mitochondrial base editors (mitoBEs). Using these upgraded mitoBEs (version 2 (v2)), we targeted 70 mouse mitochondrial DNA mutations analogous to human pathogenic variants, establishing a foundation for mitochondrial disease mouse models.
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