Journal
JOURNAL OF BONE AND MINERAL RESEARCH
Volume 29, Issue 11, Pages 2307-2322Publisher
WILEY
DOI: 10.1002/jbmr.2373
Keywords
ANIMAL MODELS; CELLS OF BONE; INJURY; FRACTURE HEALING; ORTHOPAEDICS; AGING; CELL; TISSUE SIGNALING; PARACRINE PATHWAYS; STEM AND PROGENITOR CELLS; GENETICALLY ALTERED MICE
Categories
Funding
- National Health Services [AR054041, AR48681]
Ask authors/readers for more resources
The complexity of fracture repair makes it an ideal process for studying the interplay between the molecular, cellular, tissue, and organ level events involved in tissue regeneration. Additionally, as fracture repair recapitulates many of the processes that occur during embryonic development, investigations of fracture repair provide insights regarding skeletal embryogenesis. Specifically, inflammation, signaling, gene expression, cellular proliferation and differentiation, osteogenesis, chondrogenesis, angiogenesis, and remodeling represent the complex array of interdependent biological events that occur during fracture repair. Here we review studies of bone regeneration in genetically modified mouse models, during aging, following environmental exposure, and in the setting of disease that provide insights regarding the role of multipotent cells and their regulation during fracture repair. Complementary animal models and ongoing scientific discoveries define an increasing number of molecular and cellular targets to reduce the morbidity and complications associated with fracture repair. Last, some new and exciting areas of stem cell research such as the contribution of mitochondria function, limb regeneration signaling, and microRNA (miRNA) posttranscriptional regulation are all likely to further contribute to our understanding of fracture repair as an active branch of regenerative medicine. (c) 2014 American Society for Bone and Mineral Research.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available