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Marrow Adipocyte Senescence in the Pathogenesis of Bone Loss. | LitMetric

Marrow Adipocyte Senescence in the Pathogenesis of Bone Loss.

Curr Osteoporos Rep

Division of Endocrinology, Rochester, MN, 55905, USA.

Published: August 2024

AI Article Synopsis

  • Cellular senescence is linked to various conditions beyond aging, contributing to skeletal and metabolic disorders, but the role of senescent bone marrow adipocytes (BMAds) in these issues is still under investigation.
  • Recent studies have shown senescence in BMAds due to glucocorticoid therapy, but evidence for senescence in these cells from other conditions is currently limited.
  • The review discusses the challenges of studying BMAds, highlights new techniques for their isolation and imaging, and emphasizes the potential importance of understanding BMAd senescence in relation to skeletal dysfunction and human health.

Article Abstract

Purpose Of Review: Beyond aging, senescent cells accumulate during multiple pathological conditions, including chemotherapy, radiation, glucocorticoids, obesity, and diabetes, even earlier in life. Therefore, cellular senescence represents a unifying pathogenic mechanism driving skeletal and metabolic disorders. However, whether senescent bone marrow adipocytes (BMAds) are causal in mediating skeletal dysfunction has only recently been evaluated.

Recent Findings: Despite evidence of BMAd senescence following glucocorticoid therapy, additional evidence for BMAd senescence in other conditions has thus far been limited. Because the study of BMAds presents unique challenges making these cells difficult to isolate and image, here we review issues and approaches to overcome such challenges, and present advancements in isolation and histological techniques that may help with the future study of senescent BMAds. Further insights into the roles of BMAd senescence in the pathogenesis of skeletal dysfunction may have important basic science and clinical implications for human physiology and disease.

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Source
http://dx.doi.org/10.1007/s11914-024-00875-1DOI Listing

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