Department of Cardiology, Boston Children's Hospital, Boston, Massachusetts, USA.
Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts, USA.
J Inherit Metab Dis. 2022 Jan;45(1):72-81. doi: 10.1002/jimd.12423. Epub 2021 Aug 15.
Mutation of the gene Tafazzin (TAZ) causes Barth syndrome, an X-linked disorder characterized by cardiomyopathy, skeletal muscle weakness, and neutropenia. TAZ is an acyltransferase that catalyzes the remodeling of cardiolipin, the signature phospholipid of the inner mitochondrial membrane. Here, we review the major model systems that have been established to study the role of cardiolipin remodeling in mitochondrial function and the pathogenesis of Barth syndrome. We summarize key features of each model and provide examples of how each has contributed to advance our understanding of TAZ function and Barth syndrome pathophysiology.
TAZ 基因突变导致巴陶氏症(Barth syndrome),这是一种 X 连锁的疾病,其特征为心肌病、骨骼肌无力和嗜中性白血球减少症。TAZ 是一种酰基转移酶,可催化心磷脂(cardiolipin)的重塑,心磷脂是线粒体内膜的标志性磷脂。在这里,我们回顾了已建立的主要模型系统,以研究心磷脂重塑在线粒体功能和巴陶氏症发病机制中的作用。我们总结了每个模型的主要特征,并提供了每个模型如何促进我们对 TAZ 功能和巴陶氏症病理生理学的理解的例子。