Article
Haplodeficiency of activin receptor-like kinase 4 alleviates myocardial infarction-induced cardiac fibrosis and preserves cardiac function.
Journal of molecular and cellular cardiology - 1 Apr 2017
Chen Yi-He, Wang Qian, Li Chang-Yi, Hou Jian-Wen, Chen Xiao-Meng, Zhou Qing, Chen Jie, Wang Yue-Peng, Li Yi-Gang
Abstract excerpt
Cardiac fibrosis (CF), a repairing process following myocardial infarction (MI), is characterized by abnormal proliferation of cardiac fibroblasts and excessive deposition of extracellular matrix (ECM) resulting in inevitable resultant heart failure. TGF-β (transforming growth factor-β)/ALK5 (Activin receptor-like kinase 5)/Smad2/3/4 pathways have been reported to be involved in the process. Recent studies have...
Topics
- Activin Receptors, Type I
- Animals
- Cell Movement
- Cell Proliferation
- Disease Models, Animal
- Echocardiography
- Extracellular Matrix
- Fibrosis
- Gene Expression Regulation
- Genotype
- Haploinsufficiency
- Humans
- Immunohistochemistry