Skeletal muscle inflammation and atrophy in heart failure.
Skeletal muscle inflammation and atrophy in heart failure.
复制标题
心力衰竭的骨骼肌炎症和萎缩。
DOI：
10.1007/s10741-016-9593-0
复制
发表时间：
2017-03
影响因子：
4.6
通讯作者：
Sierra OL
中科院分区：
文献类型：
--
作者：
Lavine KJ;Sierra OL
心力衰竭是一种全身性疾病，对包括骨骼肌在内的多种外周组织有深远影响。在心力衰竭的背景下，骨骼肌生理学、结构和功能的扰动强烈地促成运动不耐受和这种毁灭性疾病的发病率。越来越多的证据表明，慢性心力衰竭在骨骼肌床内引起特定的病理变化，导致肌肉功能障碍和组织萎缩。从机制上讲，全身和局部炎症反应驱动了这种病理学的关键方面。在这篇综述中，我们将讨论驱动骨骼肌炎症的病理机制，并强调位于损伤肌肉组织内的不同先天免疫亚群的新兴作用，重点是最近描述的胚胎和单核细胞衍生的巨噬细胞谱系。在此背景下，我们将讨论如何免疫机制可以有区别地针对刺激骨骼肌炎症，catalysis，纤维萎缩和再生。
Heart failure represents a systemic disease with profound effects on multiple peripheral tissues including skeletal muscle. Within the context of heart failure, perturbations in skeletal muscle physiology, structure, and function strongly contribute to exercise intolerance and the morbidity of this devastating disease. There is growing evidence that chronic heart failure imparts specific pathological changes within skeletal muscle beds resulting in muscle dysfunction and tissue atrophy. Mechanistically, systemic and local inflammatory responses drive critical aspects of this pathology. In this review, we will discuss pathological mechanisms that drive skeletal muscle inflammation and highlight emerging roles for distinct innate immune subsets that reside within damage muscle tissue focusing on the recently described embryonic and monocyte-derived macrophage lineages. Within this context, we will discuss the how immune mechanisms can be differentially targeted to stimulate skeletal muscle inflammation, catabolism, fiber atrophy, and regeneration.