Hypoxia refers to the decrease in oxygen tension in the tissues, and the central effector of the hypoxic response is the transcription factor Hypoxia-Inducible Factor α (HIF1-α). Transient hypoxia in acute events, such as exercising or regeneration after damage, play an important role in skeletal muscle physiology and homeostasis. However, sustained activation of hypoxic signaling is a feature of skeletal muscle injury and disease, which can be a consequence of chronic damage but can also increase the severity of the pathology and worsen its outcome. Here, we review evidence that supports the idea that hypoxia and HIF-1α can contribute to the establishment of fibrosis in skeletal muscle through its crosstalk with other profibrotic factors, such as Transforming growth factor β (TGF-β), the induction of profibrotic cytokines expression, as is the case of Connective Tissue Growth Factor (CTGF/CCN2), or being the target of the Renin-angiotensin system (RAS).

中文翻译：

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骨骼肌生理学和纤维化中的 HIF 缺氧信号传导。

缺氧是指组织中氧张力降低，缺氧反应的中枢效应因子是转录因子缺氧诱导因子α（HIF1-α）。急性事件中的短暂缺氧，例如运动或损伤后的再生，在骨骼肌生理学和体内平衡中起着重要作用。然而，持续激活缺氧信号是骨骼肌损伤和疾病的一个特征，这可能是慢性损伤的结果，但也会增加病理的严重程度并恶化其结果。在这里，我们回顾了支持缺氧和 HIF-1α 通过与其他促纤维化因子（例如转化生长因子 β (TGF-β)、促纤维化细胞因子的诱导）的串扰促进骨骼肌纤维化的观点的证据表达，