Molinari Francesca, Malara Natalia, Mollace Vincenzo, Rosano Giuseppe, Ferraro Elisabetta
Laboratory of Pathophysiology of Cachexia and Metabolism of Skeletal Muscle, IRCCS San Raffaele Pisana, Rome, Italy.
Interregional Research Center on Food Safety & Health (IRC-FSH), Department of Health Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy.
Int J Cardiol. 2016 Sep 15;219:105-10. doi: 10.1016/j.ijcard.2016.05.071. Epub 2016 May 31.
Cachexia is the loss of body weight associated with several chronic diseases including chronic heart failure (CHF). The cachectic condition is mainly due to loss of skeletal muscle mass and adipose tissue depletion. The majority of experimental in vivo studies on cachexia rely on animal models of cancer cachexia while a reliable and appropriate model for cardiac cachexia has not yet been established. A critical issue in generating a cardiac cachexia model is that genetic modifications or pharmacological treatments impairing the heart functionality and used to obtain the heart failure model might likely impair the skeletal muscle, this also being a striated muscle and sharing with the myocardium several molecular and physiological mechanisms. On the other hand, often, the induction of heart damage in the several existing models of heart failure does not necessarily lead to skeletal muscle loss and cachexia. Here we describe the main features of cardiac cachexia and illustrate some animal models proposed for cardiac cachexia studies; they include the genetic calsequestrin and Dahl salt-sensitive models, the monocrotaline model and the surgical models obtained by left anterior descending (LAD) ligation, transverse aortic constriction (TAC) and ascending aortic banding. The availability of a specific animal model for cardiac cachexia is a crucial issue since, besides the common aspects of cachexia in the different syndromes, each disease has some peculiarities in its etiology and pathophysiology leading to cachexia. Such peculiarities need to be unraveled in order to find new targets for effective therapies.
恶病质是与包括慢性心力衰竭（CHF）在内的多种慢性疾病相关的体重减轻。恶病质状态主要归因于骨骼肌质量的丧失和脂肪组织的消耗。大多数关于恶病质的体内实验研究依赖于癌症恶病质的动物模型，而尚未建立可靠且合适的心脏恶病质模型。建立心脏恶病质模型的一个关键问题是，用于获得心力衰竭模型的基因修饰或药物治疗损害心脏功能的同时，可能也会损害骨骼肌，因为骨骼肌也是横纹肌，与心肌共享多种分子和生理机制。另一方面，在现有的几种心力衰竭模型中，心脏损伤的诱导往往不一定会导致骨骼肌损失和恶病质。在此，我们描述心脏恶病质的主要特征，并举例说明一些用于心脏恶病质研究的动物模型；它们包括基因肌集钙蛋白和达利盐敏感模型、野百合碱模型以及通过左前降支（LAD）结扎、主动脉缩窄（TAC）和升主动脉缩窄获得的手术模型。拥有特定的心脏恶病质动物模型是一个关键问题，因为除了不同综合征中恶病质的共同方面外，每种疾病在其导致恶病质的病因和病理生理学方面都有一些独特之处。需要弄清楚这些独特之处，以便找到有效治疗的新靶点。
