Background: Muscle mitochondrial dysfunction associated with HIV and antiretroviral therapy (ART) may improve with exercise.
Methods: Muscle specimens obtained before and after 24 weeks of exercise in older people with HIV (PWH; n = 18; ART >2 years) and uninfected controls (n = 21) were analyzed for citrate synthase (CS) activity and complexes (C) I-V, manganese superoxide dismutase (MnSOD), peroxisome proliferator-activated receptor-γ coactivator-1 (PGC1α), and voltage-dependent anion channel 1 (VDAC1) content.
Results: Only controls had increased CS, MnSOD, PGC1α, and CIV (P ≤ .01; P < .01 vs PWH) after training.
Conclusions: The blunted mitochondrial adaptations to training in PWH suggests the need for different types of exercise-induced stimulation.
Clinical Trials Registration: NCT02404792.
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http://dx.doi.org/10.1093/infdis/jiaa799 | DOI Listing |
In Vivo
December 2024
College of Biology, Hunan University, Changsha, P.R. China;
Background/aim: Silicosis, the most severe type of occupational pneumoconiosis, leads to diffuse pulmonary fibrosis without specific therapy. Ferroptosis is triggered by reactive oxygen species (ROS) and Fe overload-induced lipid peroxidation, which is involved in the progression of pulmonary fibrosis. As an important coenzyme in the process of aerobic respiration, Coenzyme Q10 (CoQ10) can enhance mitochondrial function and energy supply and reduce malondialdehyde (MDA) to limit the risk of fibrosis.
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December 2024
Laboratory of Hyperspectral Imaging of Surgical Targets, Center of Excellence, L.A. Orbeli Institute of Physiology, National Academy of Sciences, Yerevan, Armenia.
Identifying factors that contribute to the transition to the dilated phase in cardiac ischemia is a critical challenge in heart failure treatment. Currently, no effective therapies exist for this ischemic complication, and the mechanisms driving left ventricular dilatation during chronic post-infarction remodeling remain poorly understood. One potential pathological process leading to ventricular dilatation involves specific compensatory rearrangements in the border zone adjacent to the infarct, which isolates the intact myocardium from inflammation at the scar edge.
View Article and Find Full Text PDFNat Commun
December 2024
Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging, Baltimore, MD, USA.
Impaired muscle mitochondrial oxidative capacity is associated with future cognitive impairment, and higher levels of PET and blood biomarkers of Alzheimer's disease and neurodegeneration. Here, we examine its associations with up to over a decade-long changes in brain atrophy and microstructure. Higher in vivo skeletal muscle oxidative capacity via MR spectroscopy (post-exercise recovery rate, k) is associated with less ventricular enlargement and brain aging progression, and less atrophy in specific regions, notably primary sensorimotor cortex, temporal white and gray matter, thalamus, occipital areas, cingulate cortex, and cerebellum white matter.
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December 2024
Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, 100091, China.
The influence of the mitochondrial control system on ischemic heart disease has become a major focus of current research. Mitophagy, as a very crucial part of the mitochondrial control system, plays a special role in ischemic heart disease, unlike mitochondrial dynamics. The published reviews have not explored in detail the unique function of mitophagy in ischemic heart disease, therefore, the aim of this paper is to summarize how mitophagy regulates the progression of ischemic heart disease.
View Article and Find Full Text PDFDrug Discov Today
December 2024
Department of Health Sciences and Biostatistics, Swinburne University of Technology, Melbourne, Australia. Electronic address:
Skeletal muscle health relies on the production of adenosine triphosphate (ATP) in the mitochondria. ATP production is accompanied by oxidative phosphorylation, which generates reactive oxygen species (ROS). When there is an imbalance in ROS levels, oxidative stress and subsequent mitochondrial dysfunction, mitochondrial myopathies including sarcopenia, chronic progressive external ophthalmoplegia, and proximal myopathy can result.
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