Division of Endocrinology, Rochester, MN, 55905, USA.
Robert and Arlene Kogod Center On Aging, Rochester, MN, 55905, USA.
Curr Osteoporos Rep. 2024 Aug;22(4):378-386. doi: 10.1007/s11914-024-00875-1. Epub 2024 Jun 3.
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.
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.
目的综述：除衰老外，衰老细胞在多种病理条件下积累，包括化疗、放疗、糖皮质激素、肥胖和糖尿病，甚至在生命早期就开始积累。因此，细胞衰老代表了驱动骨骼和代谢紊乱的统一发病机制。然而，衰老的骨髓脂肪细胞（BMAds）是否会导致骨骼功能障碍，这一点直到最近才得到评估。
最新发现：尽管有证据表明糖皮质激素治疗后会出现 BMAd 衰老，但迄今为止，其他情况下 BMAd 衰老的证据有限。由于研究 BMAds 存在独特的挑战，使得这些细胞难以分离和成像，因此，我们在这里回顾了克服这些挑战的问题和方法，并介绍了在分离和组织学技术方面的进展，这可能有助于未来对衰老的 BMAds 的研究。进一步深入了解 BMAd 衰老在骨骼功能障碍发病机制中的作用，可能对人类生理学和疾病具有重要的基础科学和临床意义。
