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Bone Marrow Skeletal Stem Cell Dysfunction: Adipocytes during skeletal aging and senescence
Aqsa Komel1,2, David Achudhan1,2, Abhishek Chandra1,2,3
1Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.
Current Opinion in Endocrine and Metabolic Research
|May 25, 2026
Summary
Cellular senescence drives skeletal stem cells (SSCs) to become bone marrow adipocytes (BMAd), increasing bone resorption. Clearing senescent cells may offer therapeutic strategies against BMAd and bone loss.
Area of Science:
- Biomedical Science
- Cell Biology
- Stem Cell Research
Background:
- Skeletal stem cells (SSCs) differentiate into various bone cells, but their fate can be skewed towards bone marrow adipocytes (BMAd).
- This skewing contributes to increased bone resorption and altered bone accrual, impacting bone health in physiological and pathological states.
- Cellular senescence, characterized by DNA damage and reactive oxygen species, is a key molecular pathway influencing SSC fate.
Purpose of the Study:
- To review the direct and indirect roles of cellular senescence in the bone marrow environment.
- To discuss how senescence influences SSC differentiation into BMAd.
- To explore therapeutic potential of targeting senescent cells for bone loss.
Main Methods:
- Literature review of preclinical studies on cellular senescence and SSC differentiation.
- Analysis of molecular pathways involved in SSC fate regulation.
- Examination of studies involving pharmacological and genetic clearance of senescent cells.
Main Results:
- Cellular senescence directly and indirectly promotes SSC differentiation into BMAd.
- Senescence-associated proinflammatory factors contribute to this altered cell fate.
- Preclinical evidence supports the clearance of senescent cells as a viable strategy.
Conclusions:
- Cellular senescence is a critical regulator of SSC fate, promoting adipogenesis over osteogenesis.
- Targeting senescent cells and their associated inflammatory signatures presents a promising therapeutic avenue.
- Mitigating BMAd accumulation through senolytic therapies could help preserve bone mass and reduce bone loss.
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