Title : Treatment of Hypertensive Heart Disease by Targeting Smad3 Signaling in Mice.

Pub. Date : 2020 Sep 11

PMID : 32953930






1 Functional Relationships(s)
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1 In addition, SIS3 treatment also halted the progression of myocardial fibrosis by blocking alpha-smooth muscle actin-positive (alpha-SMA+) myofibroblasts and collagen matrix accumulation, and inhibited cardiac inflammation by suppressing interleukin (IL)-1beta, tumor necrosis factor alpha (TNF-alpha), monocyte chemotactic protein 1 (MCP1), intercellular cell adhesion molecule-1 (ICAM1) expression, and infiltration of CD3+ T cells and F4/80+ macrophages. 6,7-dimethyl-2-(2E)-3-(1-methyl-2-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl-prop-2-enoyl)-1,2,3,4-tetrahydroisoquinoline hydrochloride actin alpha 2, smooth muscle, aorta Mus musculus