Journal article
Galectin-3 deficiency ameliorates fibrosis and remodeling in dilated cardiomyopathy mice with enhanced mst1 signaling
MN Nguyen, M Ziemann, H Kiriazis, Y Su, Z Thomas, Q Lu, DG Donner, WB Zhao, H Rafehi, J Sadoshima, JR McMullen, A El-Osta, XJ Du
American Journal of Physiology Heart and Circulatory Physiology | AMER PHYSIOLOGICAL SOC | Published : 2019
Abstract
Dilated cardio-myopathy (DCM) is a major cause of heart failure without effective therapy. Fibrogenesis plays a key role in the development of DCM, but little is known of the expression of the profibrotic factor galectin-3 (Gal-3) and its role in DCM pathophysiology. In a mouse DCM model with transgenic (TG) overexpression of mammalian sterile 20-like kinase 1 (Mst1), we studied Gal-3 expression and effects of the Gal-3 inhibitor modified citrus pectin (MCP) or Gal-3 gene knockout (KO). Gal-3 deletion in TG mice (TG/KO) was achieved by crossbreeding Mst1-TG mice with Gal-3 KO mice. The DCM phenotype was assessed by echocardiography and micromanometry. Cardiac expression of Gal-3 and fibrosis..
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Awarded by State Government of Victoria
Funding Acknowledgements
This work was supported by National Health and Medical Research Council (NHMRC) of Australia Grant ID1081710 (to X.-J. Du), the Victorian Government's Operational Infrastructure Support Program, and National Science Fund of China Grant ID81870300 (to X.-J. Du). M.-N. Nguyen was the recipient of an Australian Research Training Program Scholarship. J. R. McMullen and X.-J. Du were NHMRC fellows (ID1078985, ID1043026). W. B. Zhao and Q. Lu are funded by the China Overseas Scholarship Council (file nos. 201603170211 and 201706285111).