Department of Neuroscience, Institute of Neurology, Catholic University, Largo Agostino Gemelli 8, 00168 Rome, Italy.
Neuromuscul Disord. 2009 Nov;19(11):779-83. doi: 10.1016/j.nmd.2009.08.015. Epub 2009 Sep 20.
Caveolin-3, the myocyte-specific isoform of caveolins, is preferentially expressed in skeletal, cardiac and smooth muscles. Mutations in the CAV3 gene cause clinically heterogeneous neuromuscular disorders, including rippling muscle disease, or cardiopathies. The same mutation may lead to different phenotypes, but cardiac and muscle involvement rarely coexists suggesting that the molecular network acting with caveolin-3 in skeletal muscle and heart may differ. Here we describe an Italian family (a father and his two sons) with clinical and neurophysiological features of rippling muscle disease and heart involvement characterized by atrio-ventricular conduction defects and dilated cardiomyopathy. Muscle biopsy showed loss of caveolin-3 immunosignal. Molecular studies identified the p.A46V mutation in CAV3 previously reported in a German family with autosomal dominant rippling muscle disease and sudden death in few individuals. We suggest that cardiac dysfunction in myopathic patients with CAV3 mutations may be underestimated and recommend a more thorough evaluation for the presence of cardiomyopathy and potentially lethal arrhythmias.
窖蛋白-3(Caveolin-3)是窖蛋白家族的肌细胞特异性同工型,优先表达于骨骼肌、心肌和平滑肌。CAV3 基因突变可导致临床表现异质性的神经肌肉疾病,包括波纹肌病或心肌病。同一突变可能导致不同的表型,但心肌和肌肉受累很少同时存在,提示在骨骼肌和心脏中与窖蛋白-3 共同作用的分子网络可能不同。本文描述了一个意大利家系(父亲及其两个儿子),具有波纹肌病的临床和神经生理学特征,并伴有心脏受累,表现为房室传导缺陷和扩张型心肌病。肌肉活检显示窖蛋白-3 免疫信号缺失。分子研究发现 CAV3 中的 p.A46V 突变,该突变先前在一个德国家系中报道与常染色体显性遗传的波纹肌病和少数个体的猝死相关。我们推测 CAV3 突变的肌病患者的心脏功能障碍可能被低估,并建议更彻底地评估是否存在心肌病和潜在的致死性心律失常。