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TRPV4 as a therapeutic target for joint diseases
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  • 作者：Amy L. McNulty (1)
    Holly A. Leddy (1)
    Wolfgang Liedtke (2)
    Farshid Guilak (1)

    1. Department of Orthopaedic Surgery     ; Duke University Medical Center ; DUMC 3093 ; Durham ; NC ; 27710 ; USA
    2. Department of Neurology and Duke University Clinics for Pain and Palliative Care     ; Duke University Medical Center ; DUMC 2900 ; Durham ; NC ; 27710 ; USA
  • 关键词：Mechanotransduction ; Proteinase ; activated receptor 2 ; Chondrocyte ; Osteoblast ; Osteoclast ; Tissue engineering
  • 刊名：Naunyn-Schmiedeberg's Archives of Pharmacology
  • 出版年：2015
  • 出版时间：April 2015
  • 年：2015
  • 卷：388
  • 期：4
  • 页码：437-450
  • 全文大小：2,246 KB
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  • 刊物类别：Biomedical and Life Sciences
  • 刊物主题：Biomedicine
    Pharmacology and Toxicology
    Neurosciences
  • 出版者：Springer Berlin / Heidelberg
  • ISSN：1432-1912
文摘
Biomechanical factors play a critical role in regulating the physiology as well as the pathology of multiple joint tissues and have been implicated in the pathogenesis of osteoarthritis. Therefore, the mechanisms by which cells sense and respond to mechanical signals may provide novel targets for the development of disease-modifying osteoarthritis drugs (DMOADs). Transient receptor potential vanilloid 4 (TRPV4) is a Ca2+-permeable cation channel that serves as a sensor of mechanical or osmotic signals in several musculoskeletal tissues, including cartilage, bone, and synovium. The importance of TRPV4 in joint homeostasis is apparent in patients harboring TRPV4 mutations, which result in the development of a spectrum of skeletal dysplasias and arthropathies. In addition, the genetic knockout of Trpv4 results in the development of osteoarthritis and decreased osteoclast function. In engineered cartilage replacements, chemical activation of TRPV4 can reproduce many of the anabolic effects of mechanical loading to accelerate tissue growth and regeneration. Overall, TRPV4 plays a key role in transducing mechanical, pain, and inflammatory signals within joint tissues and thus is an attractive therapeutic target to modulate the effects of joint diseases. In pathological conditions in the joint, when the delicate balance of TRPV4 activity is altered, a variety of different tools could be utilized to directly or indirectly target TRPV4 activity.

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