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Heat Shock Proteins in Tendinopathy: Novel Molecular Regulators

机译:肌腱病变中的热休克蛋白质:新型分子调节剂

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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.
机译:肌腱紊乱 - 肌腱病变 - 是初级保健中肌肉骨骼咨询的主要原因,占高达30%的风湿病学咨询。虽然肌腱病变的分子病理生理学仍然难以解释涉及重复应激的疾病过程,但细胞载荷为跨越自身免疫群落中许多疾病过程的热休克蛋白区域提供了重要的机制洞察。热休克蛋白,也称为损伤相关的分子模式(潮湿),在非程序性细胞死亡之后迅速释放,是先天免疫系统的关键效应,并通过促进效果组织的重建来重视稳定性。我们的调查强调了HSP在招疾病中的关键作用,这最终可能影响肌腱病理学中的组织救援机制。本文旨在概述软组织中的热休克蛋白质的生物学以及这些介质如何成为煽动性介质的重要调节因子和肌腱病变中的基质调节。

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