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Updated: May 11, 2026

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
Suppression of autophagy in osteocytes mimics skeletal aging
Melda Onal1, Marilina Piemontese, Jinhu Xiong
1Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Abstract:
Bone mass declines with age but the mechanisms responsible remain unclear. Here we demonstrate that deletion of a conditional allele for Atg7, a gene essential for autophagy, from osteocytes caused low bone mass in 6-month-old male and female mice. Cancellous bone volume and cortical thickness were decreased, and cortical porosity increased, in conditional knock-out mice compared with control littermates. These changes were associated with low osteoclast number, osteoblast number, bone formation rate, and wall width in the cancellous bone of conditional knock-out mice. In addition, oxidative stress was higher in the bones of conditional knock-out mice as measured by reactive oxygen species levels in the bone marrow and by p66(shc) phosphorylation in L6 vertebra. Each of these changes has been previously demonstrated in the bones of old versus young adult mice. Thus, these results demonstrate that suppression of autophagy in osteocytes mimics, in many aspects, the impact of aging on the skeleton and suggest that a decline in autophagy with age may contribute to the low bone mass associated with aging.
Insights
Autophagy, a cellular recycling process, is crucial for maintaining bone mass. Suppressing autophagy in bone cells mimics aging, leading to reduced bone density and increased bone fragility.
Area of Science:
- Cell Biology
- Bone Biology
- Aging Research
Background:
- Bone mass naturally decreases with age, but the underlying mechanisms are not fully understood.
- Autophagy is a vital cellular process for maintaining cellular health and homeostasis.
- Osteocytes, the primary cells within bone, play a critical role in bone remodeling and maintenance.
Purpose of the Study:
- To investigate the role of autophagy in osteocytes in regulating bone mass.
- To determine if impaired autophagy in osteocytes contributes to age-related bone loss.
Main Methods:
- Conditional deletion of the Atg7 gene (essential for autophagy) in mouse osteocytes.
- Analysis of bone mass, microarchitecture, and cellular activity (osteoblasts and osteoclasts) in genetically modified mice.
- Assessment of oxidative stress markers in bone tissue.
Main Results:
- Deletion of Atg7 in osteocytes led to significantly reduced bone mass and altered bone microarchitecture (decreased cancellous bone volume and cortical thickness, increased porosity).
- These bone changes were associated with reduced osteoblast and osteoclast numbers and decreased bone formation rates.
- Elevated levels of oxidative stress markers were observed in the bones of mice with impaired autophagy in osteocytes.
Conclusions:
- Suppression of autophagy in osteocytes significantly impacts bone mass and structure, mimicking many aspects of age-related bone loss.
- A decline in autophagy within osteocytes may be a contributing factor to the reduced bone mass observed during aging.
- Targeting autophagy in osteocytes could represent a potential therapeutic strategy for age-related bone diseases.
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