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Mediators of Inflammation
Volume 2012 (2012), Article ID 436203, 7 pages
Review Article

Heat Shock Proteins in Tendinopathy: Novel Molecular Regulators

1Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK
2Department of Orthopaedic Surgery, Orthopaedic Research Institute, University of New South Wales, St. George Hospital Campus, Kogarah, Sydney, NSW 2217, Australia

Received 30 July 2012; Accepted 25 September 2012

Academic Editor: Chiara De Luca

Copyright © 2012 Neal L. Millar and George A. C. Murrell. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Tendon disorders—tendinopathies—are the primary reason for musculoskeletal consultation in primary care and account for up to 30% of rheumatological consultations. Whilst the molecular pathophysiology of tendinopathy remains difficult to interpret the disease process involving repetitive stress, and cellular load provides important mechanistic insight into the area of heat shock proteins which spans many disease processes in the autoimmune community. Heat shock proteins, also called damage-associated molecular patterns (DAMPs), are rapidly released following nonprogrammed cell death, are key effectors of the innate immune system, and critically restore homeostasis by promoting the reconstruction of the effected tissue. Our investigations have highlighted a key role for HSPs in tendion disease which may ultimately affect tissue rescue mechanisms in tendon pathology. This paper aims to provide an overview of the biology of heat shock proteins in soft tissue and how these mediators may be important regulators of inflammatory mediators and matrix regulation in tendinopathy.