Desdín-Micó et al. have shown that Tfam specific knockout in mouse T cells disrupts mitochondrial genome integrity and induces a burst of inflammatory cytokines and tumor necrosis factor (TNF)-α production, resulting in increased senescence, neuromuscular and vascular dysfunction, and molecular features that recapitulate premature aging. Interestingly, treatment with nicotinamide riboside (NR) alleviates this phenotype by reducing senescence and systemic inflammation.
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http://dx.doi.org/10.1016/j.molmed.2020.07.001 | DOI Listing |
J Cell Sci
January 2025
Department of Biomedical Engineering, Northwestern University, Evanston, Illinois, 60208, USA.
Disrupted nuclear shape is associated with multiple pathological processes including premature aging disorders, cancer-relevant chromosomal rearrangements, and DNA damage. Nuclear blebs (i.e.
View Article and Find Full Text PDFFront Immunol
January 2025
Division for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, Ulm University Medical Center, Ulm, Germany.
Background: The complement system is locally activated after joint injuries and leads to the deposition of the terminal complement complex (TCC). Sublytic TCC deposition is associated with phenotypical alterations of human articular chondrocytes (hAC) and enhanced release of inflammatory cytokines. Chronic inflammation is a known driver of chondrosenescence in osteoarthritis (OA).
View Article and Find Full Text PDFGeroscience
January 2025
State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Hong Kong, China.
Biological brain age is a brain-predicted age using machine learning to indicate brain health and its associated conditions. The presence of an older predicted brain age relative to the actual chronological age is indicative of accelerated aging processes. Consequently, the disparity between the brain's chronological age and its predicted age (brain-age gap) and the factors influencing this disparity provide critical insights into cerebral health dynamics during aging.
View Article and Find Full Text PDFAging Cell
January 2025
Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados, Ciudad de México, Mexico.
Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease caused by progerin, a mutant variant of lamin A. Progerin anchors aberrantly to the nuclear envelope disrupting a plethora of cellular processes, which in turn elicits senescence. We previously showed that the chromosomal region maintenance 1 (CRM1)-driven nuclear export pathway is abnormally enhanced in patient-derived fibroblasts, due to overexpression of CRM1.
View Article and Find Full Text PDFCell Biosci
January 2025
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.
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