Article
Interleukin-18 deteriorates Fabry cardiomyopathy and contributes to the development of left ventricular hypertrophy in Fabry patients with GLA IVS4+919 G>A mutation.
Oncotarget - 27 Dec 2016
Chien Yueh, Chien Chian-Shiu, Chiang Huai-Chih, Huang Wei-Lin, Chou Shih-Jie, Chang Wei-Chao, Chang Yuh-Lih, Leu Hsin-Bang, Chen Kuan-Hsuan, Wang Kang-Ling, Lai Ying-Hsiu, Liu Yung-Yang, Lu Kai-Hsi, Li Hsin-Yang, Sung Yen-Jen, Jong Yuh-Jyh, Chen Yann-Jang, Chen Chung-Hsuan, Yu Wen-Chung
Abstract excerpt
RATIONALE: A high incidence of GLA IVS4+919 G>A mutation in patients with Fabry disease of the later-onset cardiac phenotype, has been reported in Taiwan. However, suitable biomarkers or potential therapeutic surrogates for Fabry cardiomyopathy (FC) in such patients under enzyme replacement treatment (ERT) remain unknown. OBJECTIVE: Using FC patients carrying IVS4+919 G>A mutation, we constructed an induced...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
