Journal
SKELETAL BIOLOGY AND MEDICINE II: BONE AND CARTILAGE HOMEOSTASIS AND BONE DISEASE
Volume 1240, Issue -, Pages 32-37Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/j.1749-6632.2011.06301.x
Keywords
mechanical loading; osteoarthritis; exercise; cartilage degradation
Funding
- NIH [AR47628, AR52743]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR052743, R01AR050968, R03AR047628] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Osteoarthritis (OA) is characterized by the breakdown of articular cartilage that is mediated in part by increased production of matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS), enzymes that degrade components of the cartilage extracellular matrix. Efforts to design synthetic inhibitors of MMPs/ADAMTS have only led to limited clinical success. In addition to pharmacologic therapies, physiologic joint loading is widely recommended as a nonpharmacologic approach to improve joint function in osteoarthritis. Clinical trials report that moderate levels of exercise exert beneficial effects, such as improvements in pain and physical function. Experimental studies demonstrate that mechanical loading mitigates joint destruction through the downregulation of MMPs/ADAMTS. However, the molecular mechanisms underlying these effects of physiologic loading on arthritic joints are not well understood. We review here the recent progress on mechanotransduction in articular joints, highlighting the mediators and pathways in the maintenance of cartilage integrity, especially in the prevention of cartilage degradation in OA.
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