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• W4377029292 abstract "<b>Abstract ID 13843</b> <b>Poster Board 51</b> Mitochondria are active organelles, undergoing harmonized cycles of fission and fusion, driven by 9mitochondrial dynamics,9 to retain their morphology, distribution, and size. Mitochondrial dynamics has emerged as a critical process in maintaining cellular homeostasis. Interestingly, it has been long respected that a decrease in mitochondrial function escorts aging in specific tissues. For example, skeletal muscle gradually loses mass, strength, endurance, and oxidative capacity during aging. This decrease might, in turn, contribute to the observed age-dependent decline in organ function by mutations or alterations in mitochondrial fusion and fission proteins associated with several diseases. However, new players in regulating mitochondrial shape and cristae shape have been recently studied, such as the mitochondrial contact site and cristae organizing system (MICOS) complex. The MICOS complex is a multi-protein interaction hub that helps define cristate and mitochondria architecture. However, the MICOS complex has not been implicated in regulating organelle structure changes during aging. Thus, we hypothesized that loss of the MICOS complex during aging may increase mitochondrial fragmentation, decrease nanotunnels, and alter cristae morphology. To do this, we examined the three-dimensional morphology of mitochondria networks in young (3-month) and aged (2-year) murine gastrocnemius muscle via serial block face-scanning electron microscopy and the Amira program for segmentation, analysis, and quantification. We found differences in mitochondrial network configuration, nanotunneling, size, shape, number, contact sites, and MICOS gene expression in skeletal muscle during aging. We also found an association between OPA-1 and the MICOS complex in the gastrocnemius with mitochondrial aging. Furthermore, the loss of the MICOS complex was linked with decreased oxidative capacity and altered mitochondrial metabolism. Importantly, this highlights the importance of investigating the repair of muscle using novel mitochondrial therapies. For example, activating transcription factor-4 (ATF4) may be able to restore mitochondrial cristae integrity. Together, these results suggest a novel relationship between the MICOS complex and aging in skeletal muscle. Support/Funding Information: The United Negro College Fund/Bristol-Myers Squibb E.E. Just Faculty Fund, BWF Career Awards at the Scientific Interface Award, BWF Ad-hoc Award, NIH Small Research Pilot Subaward to 5R25HL106365-12 from the National Institutes of Health PRIDE Program, DK020593, Vanderbilt Diabetes and Research Training Center for DRTC Alzheimer9s Disease Pilot & Feasibility Program. CZI Science Diversity Leadership grant number 2022- 253529 from the Chan Zuckerberg Initiative DAF, an advised fund of Silicon Valley Community Foundation." @default.
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• W4377029292 date "2023-05-18" @default.
• W4377029292 modified "2023-10-18" @default.
• W4377029292 title "3D Reconstruction Reveals Changes in Mitochondrial Morphology in Mouse Skeletal Muscle Across Aging and Upon Loss of the MICOS Complex" @default.
• W4377029292 doi "https://doi.org/10.1124/jpet.122.138430" @default.
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