期刊
RHEUMATOLOGY
卷 52, 期 5, 页码 769-779出版社
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/kes409
关键词
alarmins; tendinopathy; inflammation; cytokines; hypoxia
类别
资金
- Arthritis Research UK Orthopaedic Clinical Research Fellowship
- Royal College of Surgeons of Edinburgh Cutner Fellowship
- Academy of Medical Sciences (AMS) [AMS-SGCL8-Millar] Funding Source: researchfish
- Versus Arthritis [20086] Funding Source: researchfish
Tendon disorders-tendinopathies-are the primary reason for musculoskeletal consultation in primary care in the UK and account for up to 30% of rheumatological consultations. While the molecular pathophysiology of tendinopathy remains incompletely understood, recent observations concerning repetitive stress and cellular load provide important mechanistic insight implicating a role for tissue alarmins. These in turn have an emerging effector role in many disease processes across the rheumatological diseases. Intracellular alarmins, also called damage-associated molecular patterns, are rapidly released following non-programmed cell death, are key effectors of the innate immune system and critically restore homeostasis by promoting the reconstruction of the affected tissue. Recent investigations have highlighted a key role for several alarmins including hypoxia-induced elements, cytokines and heat shock proteins affecting tissue rescue mechanisms in tendon pathology. This review aims to provide an overview of the biology of alarmins in the context of inflammatory mediators and matrix regulation in tendinopathy.
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