Exercise to Mend Aged-tissue Crosstalk in Bone Targeting Osteoporosis & Osteoarthritis.

Autor: Little-Letsinger SE; Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina at Chapel Hill, NC, USA., Rubin J; Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina at Chapel Hill, NC, USA; North Carolina Diabetes Research Center (NCDRC), University of North Carolina at Chapel Hill, NC, USA; Department of Medicine, Thurston Arthritis Research Center (TARC), University of North Carolina at Chapel Hill, NC, USA., Diekman B; Department of Medicine, Thurston Arthritis Research Center (TARC), University of North Carolina at Chapel Hill, NC, USA; Joint Departments of Biomedical Engineering NC State & University of North Carolina at Chapel Hill, NC, USA., Rubin CT; Department of Biomedical Engineering, State University of New York at Stony Brook, NY, NY, USA., McGrath C; Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina at Chapel Hill, NC, USA., Pagnotti GM; Department of Endocrine, Neoplasia, and Hormonal Disorders, University of Texas MD Anderson Cancer Center, Houston, TX, USA., Klett EL; Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina at Chapel Hill, NC, USA; Department of Nutrition, School of Public Health, University of North Carolina at Chapel Hill, NC, USA., Styner M; Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina at Chapel Hill, NC, USA; North Carolina Diabetes Research Center (NCDRC), University of North Carolina at Chapel Hill, NC, USA; Department of Medicine, Thurston Arthritis Research Center (TARC), University of North Carolina at Chapel Hill, NC, USA. Electronic address: mstyner@unc.edu.
Jazyk: angličtina
Zdroj: Seminars in cell & developmental biology [Semin Cell Dev Biol] 2022 Mar; Vol. 123, pp. 22-35. Date of Electronic Publication: 2021 Sep 04.
DOI: 10.1016/j.semcdb.2021.08.011
Abstrakt: Aging induces alterations in bone structure and strength through a multitude of processes, exacerbating common aging- related diseases like osteoporosis and osteoarthritis. Cellular hallmarks of aging are examined, as related to bone and the marrow microenvironment, and ways in which these might contribute to a variety of age-related perturbations in osteoblasts, osteocytes, marrow adipocytes, chondrocytes, osteoclasts, and their respective progenitors. Cellular senescence, stem cell exhaustion, mitochondrial dysfunction, epigenetic and intracellular communication changes are central pathways and recognized as associated and potentially causal in aging. We focus on these in musculoskeletal system and highlight knowledge gaps in the literature regarding cellular and tissue crosstalk in bone, cartilage, and the bone marrow niche. While senolytics have been utilized to target aging pathways, here we propose non-pharmacologic, exercise-based interventions as prospective "senolytics" against aging effects on the skeleton. Increased bone mass and delayed onset or progression of osteoporosis and osteoarthritis are some of the recognized benefits of regular exercise across the lifespan. Further investigation is needed to delineate how cellular indicators of aging manifest in bone and the marrow niche and how altered cellular and tissue crosstalk impact disease progression, as well as consideration of exercise as a therapeutic modality, as a means to enhance discovery of bone-targeted therapies.
(Copyright © 2021. Published by Elsevier Ltd.)
Databáze: MEDLINE
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