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Dysfunctional stem and progenitor cells impair fracture healing with age

World Journal of Stem Cells 2019年第6期11卷 281-296页

作者： Diane R Wagner Sonali Karnik Zachary J Gunderson Jeffery J Nielsen Alanna Fennimore Hunter J Promer Jonathan W Lowery M Terry Loghmani Philip S Low todd o mckinley Melissa A Kacena Matthias Clauss Jiliang Li Department of Mechanical and Energy Engineering Indiana University-Purdue University IndianapolisIndianapolisIN 46202United States Department of orthopaedic Surgery Indiana University School of MedicineIndianapolisIN 46202United States Department of Medicinal Chemistry and Molecular Pharmacology Purdue UniversityWest LafayetteIN 47907United States Department of Physical Therapy Indiana University- Purdue University IndianapolisIndianapolisIN 46202United States Division of Biomedical Science Marian University College of Osteopathic MedicineIndianapolisIN 46222United States Department of Chemistry Purdue UniversityWest LafayetteIN 47907 United States Richard L. Roudebush VA Medical Center IndianapolisIN 46202United States Department of Medicine Indiana University School of MedicineIndianapolisIN 46202United States Department of Biology Indiana University-Purdue University IndianapolisIndianapolisIN 46202United States

Successful fracture healing requires the simultaneous regeneration of both the bone and vasculature;mesenchymal stem cells (MSCs) are directed to replace the bone tissue, while endothelial progenitor cells (EPCs) form the new vasculature that supplies blood to the fracture site. In the elderly, the healing process is slowed, partly due to decreased regenerative function of these stem and progenitor cells. MSCs from older individuals are impaired with regard to cell number, proliferative capacity, ability to migrate, and osteochondrogenic differentiation potential. The proliferation, migration and function of EPCs are also compromised with advanced age. Although the reasons for cellular dysfunction with age are complex and multidimensional, reduced expression of growth factors, accumulation of oxidative damage from reactive oxygen species, and altered signaling of the Sirtuin-1 pathway are contributing factors to aging at the cellular level of both MSCs and EPCs. Because of these geriatric-specific issues, effective treatment for fracture repair may require new therapeutic techniques to restore cellular function. Some suggested directions for potential treatments include cellular therapies, pharmacological agents, treatments targeting age-related molecular mechanisms, and physical therapeutics. Advanced age is the primary risk factor for a fracture, due to the low bone mass and inferior bone quality associated with aging;a better understanding of the dysfunctional behavior of the aging cell will provide a foundation for new treatments to decrease healing time and reduce the development of complications during the extended recovery from fracture healing in the elderly.

关键词： Fracture healing Aging Bone Angiogenesis Mesenchymal stem cells Endothelial progenitor cells

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