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Mitochondria are double membrane-bound organelles with pleiotropic roles in the cell, including energy production through aerobic respiration, calcium signaling, metabolism, proliferation, immune signaling, and apoptosis. Dysfunction of mitochondria is associated with numerous physiological consequences and drives various diseases, and is one of twelve biological hallmarks of aging, linked to aging pathology. There are many distinct changes that occur to the mitochondria during aging including changes in mitochondrial morphology, which can be used as a robust and simple readout of mitochondrial quality and function. Although mitochondrial morphology alone cannot be used to conclude the quality of mitochondria, it is highly correlated with mitochondrial function whereby mitochondria exhibit increased fragmentation with age in multiple cell types of the nematode . Thus, serve as a robust model for rapidly measuring mitochondrial morphology changes during aging. To standardize imaging methods for mitochondrial morphology in , we provide a detailed comparative characterization of several transgenic constructs, highlighting benefits and caveats for aging biology studies.
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http://dx.doi.org/10.1101/2024.12.24.630282 | DOI Listing |
Med Oncol
September 2025
Venom and Biotherapeutics Molecules Laboratory, Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.
Neuropeptide Y (NPY) and the voltage-gated potassium channel Kv1.3 are closely associated with breast cancer progression and apoptosis regulation, respectively. NPY receptors (NPYRs), which are overexpressed in breast tumors, contribute to tumor growth, migration, and angiogenesis.
View Article and Find Full Text PDFMol Biomed
September 2025
National Key Laboratory of Immunity and Inflammation & Institute of Immunology, College of Basic Medical Sciences, Naval Medical University, Shanghai, 200433, China.
Dendritic cells (DCs) play a central role in coordinating immune responses by linking innate and adaptive immunity through their exceptional antigen-presenting capabilities. Recent studies reveal that metabolic reprogramming-especially pathways involving acetyl-coenzyme A (acetyl-CoA)-critically influences DC function in both physiological and pathological contexts. This review consolidates current knowledge on how environmental factors, tumor-derived signals, and intrinsic metabolic pathways collectively regulate DC development, subset differentiation, and functional adaptability.
View Article and Find Full Text PDFFASEB J
September 2025
Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Engineering Research Center of Oral Biomaterials
The onset and progression of periodontitis are closely related to metabolic reprogramming in the periodontal microenvironment, with osteoclasts playing a critical role in tissue destruction. Single-cell RNA sequencing (scRNA-seq) of periodontal tissues from healthy individuals and patients with severe chronic periodontitis revealed a significant increase in the expression of mitochondrial-related genes during osteoclast differentiation, suggesting the critical role of mitochondrial function in this process. This study investigates the potential of the novel mitoribosome-targeting antibiotic radezolid in inhibiting osteoclast differentiation.
View Article and Find Full Text PDFJCI Insight
September 2025
Division of Cardiovascular Medicine, Department of Medicine.
Aortic valve stenosis is a progressive and increasingly prevalent disease in older adults, with no approved pharmacologic therapies to prevent or slow its progression. Although genetic risk factors have been identified, the contribution of epigenetic regulation remains poorly understood. Here, we demonstrated that histone deacetylase 3 (HDAC3) maintains aortic valve structure by suppressing mitochondrial biogenesis and preserving extracellular matrix integrity in valvular interstitial fibroblasts.
View Article and Find Full Text PDFJCI Insight
September 2025
Alice and Y. T. Chen Center for Genetics and Genomics, Division of Medical Genetics, Department of Pediatrics.
Methylmalonic acidemia (MMA) is a severe metabolic disorder affecting multiple organs because of a distal block in branched-chain amino acid (BCAA) catabolism. Standard of care is limited to protein restriction and supportive care during metabolic decompensation. Severe cases require liver/kidney transplantation, and there is a clear need for better therapy.
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