Tendinopathy is the most common disorder in sports medicine. Multiple hypotheses have been proposed for the aetiopathogenesis, but many aspects still remain elusive. Microdialysis studies have shown high levels of lactate within tendinosis, even at resting tendons,1 suggesting that hypoxia persists in tendinopathy. The presence of necrotic tenocytes, blocked arteries and anaerobic enzymes within tendinopathy lesions lend further support to the role of hypoxia in the aetiopathogenesis.2 Finally, ‘tendinosis’, the pathognomonic histopathological finding in tendinopathy, is composed of hypoxic, mucoid, hyaline and fibrinoid tissue.2 These tissue types are known to be hypoxia induced. Tendons are generally poorly vascularised, while certain regions—those most prone to injury—are almost avascular. This can be considered an evolutionary ‘design failure’ that makes tendons susceptible to chronic and acute injuries. As a consequence, healthy tendons have a virtually non-existent tissue turnover throughout adulthood.3 However, somewhat paradoxically, tissue turnover is increased in tendinopathic tendons.3 Given the persisting hypoxia and subsequent anaerobic metabolism,1 2 it comes as no surprise that the enhanced tissue turnover leads to production of poorly organised tissue—tendinosis—in tendinopathy.2 The fundamental survival mechanism of any cell under hypoxia is the activation of hypoxia-inducible factor-1α (HIF-1α),4 a transcription factor that turns …

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肌腱病中的新生血管形成：从根除到稳定？

肌腱病是运动医学中最常见的疾病。已经对发病机制提出了多种假设，但许多方面仍然难以捉摸。微透析研究表明，肌腱病内的乳酸水平很高，即使在静止的肌腱处，1 表明肌腱病中持续存在缺氧。肌腱病病变内坏死的肌腱细胞、动脉阻塞和厌氧酶的存在进一步支持了缺氧在发病机制中的作用。2 最后，“肌腱病”是肌腱病的病理组织学发现，由缺氧、粘液、透明和纤维蛋白组成组织。2 已知这些组织类型是缺氧诱导的。肌腱的血管化通常很差，而某些区域——最容易受伤的区域——几乎没有血管。这可以被认为是一种进化的“设计失败”，使肌腱容易受到慢性和急性损伤。因此，健康肌腱在整个成年期几乎不存在组织更新。3 然而，有点矛盾的是，肌腱病肌腱的组织更新增加了。3 鉴于持续缺氧和随后的无氧代谢，1 2 也就不足为奇了增强的组织周转会导致肌腱病中组织不良的组织——肌腱变性。2 缺氧条件下任何细胞的基本生存机制是激活缺氧诱导因子 1α (HIF-1α)，4 是一种转录因子，它会转变……