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Cellular Communication in Bone Homeostasis and the Related Anti-osteoporotic Drug Development
Yi Zhang1, Guojing Luo1, Xijie Yu1
1Laboratory of Endocrinology and Metabolism, Department of Endocrinology and Metabolism, National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.
Current Medicinal Chemistry
|August 3, 2018
Summary
Disrupted bone cell communication causes osteoporosis. Understanding these signals offers new therapeutic targets beyond current treatments, aiming for better osteoporosis management.
Area of Science:
- Bone Biology
- Cellular Signaling
- Metabolic Bone Diseases
Background:
- Bone homeostasis relies on intricate crosstalk between osteoblasts, osteoclasts, osteocytes, and chondrocytes.
- Dysregulation of this cellular and molecular signaling pathway is implicated in metabolic bone disorders like osteoporosis.
- Existing osteoporosis interventions face limitations due to side effects, complications, and poor long-term tolerance.
Purpose of the Study:
- To review intercellular communication mechanisms governing bone remodeling.
- To explore the potential of targeting bone cell signaling for novel osteoporosis drug development.
Main Methods:
- A comprehensive literature search of PubMed from 1980 to 2018 was conducted.
- Keywords included 'osteoporosis,' 'bone remodeling,' and various bone cell types and therapeutic agents.
- 170 relevant publications were selected for review, focusing on cell interactions and therapeutic strategies.
Main Results:
- Approximately 80 papers detailed the complex bone cell interactions crucial for bone remodeling.
- The remaining publications focused on emerging and advanced osteoporosis therapies.
- A complex signaling network among bone cells is essential for maintaining bone remodeling.
Conclusions:
- Disordered cell-to-cell communication is a potential underlying mechanism in osteoporosis.
- Current osteoporosis treatments are effective but have associated drawbacks.
- Developing individualized therapies that restore abnormal signaling networks is key for optimal drug development.
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