Pharmaceutical composition for treatment of cardiac fibrosis

Abstract

The invention relates to a pharmaceutical composition for the treatment of cardiac fibrosis or heart diseases accompanied by cardiac fibrosis. According to the invention, the composition of the invention has an effect of dissolving a fibrosis matrix and performing restoration to normal tissues by selectively destroying myofibroblasts in cardiac fibrosis which is diagnosed after a disease occurs, and therefore can be usefully used as a composition for the treatment of cardiac fibrosis, systolic heart failure and diastolic heart failure for which a therapeutic agent has not been developed due tobeing considered as an irreversible disease progression up to date.

Description

technical field [0001] This patent application claims the benefit of priority from Korean Patent Application No. 10-2015-015988 filed with the Korean Intellectual Property Office on November 13, 2015, the contents of which are incorporated herein by reference in their entirety. [0002] The present invention relates to a pharmaceutical composition for treating cardiac fibrosis, more particularly, to a pharmaceutical composition for treating cardiac fibrosis or heart diseases accompanied by cardiac fibrosis. Background technique [0003] Rare diseases developed in the treatment of fibrosis arise from the differentiation of fibroblasts present in cardiac tissue, vascular endothelial cells, and bone marrow cells. Although the source cells of myofibroblasts may be different, differentiated myofibroblasts are involved in the overproduction of extracellular matrix such as fibrotic collagen and its secretion. Degeneration of contractile cells due to expression of intracellular α-s...

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2) Passive tissue stiffness increases due to cross-linking of secreted type 1 collagen and gap junctions of myofibroblasts, resulting in the generation of contractile fibrous tissue leading to diastolic dysfunction (Lo B. et al. Hypertension 60:677683( 2012))

In each of the transgenic model mice, the endothelial-mesenchymal transition (EndoMT) of vascular endothelial cells to myofibroblasts was inhibited, which showed the effect of preventing the deterioration of cardiac function that progressed to cardiac fibrosis and heart failure, but it has not been confirmed Produced a therapeutic effect on fibrosis (Okayama K., Azuma J., et al.Hypertension 59(5):958-965(2012); and Kapur N.K., et al.Circulation 125(22):2728-2738(2012 ))

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