Metabolic Regulators of Bone Health
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".
Deadline for manuscript submissions: 20 March 2026 | Viewed by 856
Special Issue Editor
Interests: regenerative medicine; tissue engineering; 3D bioprinting; biomaterials; bone; cartilage; skin; inflammation; differentiation
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Metabolic regulation plays a crucial role in bone health, with conditions such as osteoporosis, obesity, and diabetes significantly impacting skeletal integrity. Metabolic factors, including glucose, insulin, estrogen, and lipids, influence bone-building cells osteoblasts affecting their osteogenic potential and overall bone homeostasis. Dysregulated glucose and lipids metabolism and insulin signaling have been linked to impaired bone formation, while estrogen deficiency accelerates bone loss, contributing to osteoporosis. In recent years, numerous signaling pathways and microRNAs have been associated with metabolic regulation in bone biology. Future research should aim to systematically elucidate the molecular mechanisms underlying these metabolic influences on bone health, particularly by investigating the crosstalk between osteoblasts, osteocytes, and these microenvironmental factors.
In this Special Issue of IJMS, we will focus on molecular studies in bone biology and regenerative medicine as a promising approach to identifying new therapeutic targets and biomarkers with diagnostic significance in metabolic bone disorders. We welcome in vitro data, human studies, and clinical observations that explore the effects of metabolic regulators on bone health, with a particular emphasis on glucose, insulin, lipids, and estrogen signaling in bone-forming cells.
Dr. Akkouch Adil
Guest Editor
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Keywords
- bone
- osteoporosis
- diabetes
- obesity
- glucose
- insulin
- lipids
- estrogen
- microRNA
- osteoblasts
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