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

Pub. Date : 2020 Sep 11

PMID : 32953930






3 Functional Relationships(s)
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1 Because Smad7 functions as an inhibitor for both TGF-beta/Smad and nuclear factor kappaB (NF-kappaB) signaling, increased cardiac Smad7 could be another mechanism through which SIS3 treatment blocked Smad3-mediated myocardial fibrosis and NF-kappaB-driven cardiac inflammation. 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 SMAD family member 7 Mus musculus
2 Because Smad7 functions as an inhibitor for both TGF-beta/Smad and nuclear factor kappaB (NF-kappaB) signaling, increased cardiac Smad7 could be another mechanism through which SIS3 treatment blocked Smad3-mediated myocardial fibrosis and NF-kappaB-driven cardiac inflammation. 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 SMAD family member 7 Mus musculus
3 Because Smad7 functions as an inhibitor for both TGF-beta/Smad and nuclear factor kappaB (NF-kappaB) signaling, increased cardiac Smad7 could be another mechanism through which SIS3 treatment blocked Smad3-mediated myocardial fibrosis and NF-kappaB-driven cardiac inflammation. 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 SMAD family member 7 Mus musculus