| Gene | Score gda | Association Type | Type | Original DB | Sentence supporting the association | PMID | PMID Year | ||||
|---|---|---|---|---|---|---|---|---|---|---|---|
|
0.070 | Biomarker | disease | BEFREE | Furthermore, expressions of TGF-β1, p-Smad3 and p-GSK-3β were significantly decreased in the QSG treatment group compared with the model group, suggesting that the QSG may attenuate cardiac fibrosis through regulating TGF-β/Smad3 pathway. | 31102891 | 2019 | ||||
|
0.070 | Biomarker | disease | BEFREE | Long noncoding RNA Crnde attenuates cardiac fibrosis via Smad3-Crnde negative feedback in diabetic cardiomyopathy. | 30748104 | 2019 | ||||
|
0.070 | Biomarker | disease | BEFREE | Further studies revealed that YWPC could inhibit DOX-induced cardiac fibrosis through inhibiting TGF-β/smad3-mediated ECM synthesis. | 31225944 | 2019 | ||||
|
0.070 | Biomarker | disease | BEFREE | Oxidative stress, endoplasmic reticulum (ER) stress, and canonical Smad3 pathway are implicated in the pathogenesis of cardiac fibrosis. | 30123131 | 2018 | ||||
|
0.070 | Biomarker | disease | BEFREE | Heat shock transcription factor 1 protects against pressure overload-induced cardiac fibrosis via Smad3. | 28091697 | 2017 | ||||
|
0.070 | Biomarker | disease | BEFREE | Here we report: 1) In a wild-type mouse model of MI, ALK4 upregulation was restricted in the fibroblasts of the infarct border zone; 2) In contrast, ALK4<sup>+/-</sup> mice with a haplodeficiency of ALK4 gene, showed a significantly attenuated CF in the border zone, with a smaller scar size, a preserved cardiac function and an improved survival rate post-MI; 3) Similarly to pressure-overloaded heart, these beneficial effects might be through a partial inactivation of the Smad3/4 pathway but not MAPK cascades; 4) The apoptotic rate of the cardiomyocytes were indistinguishable in the border zone of the wild-type control and ALK4<sup>+/-</sup> mice; 5) Cardiac fibroblasts isolated from ALK4<sup>+/-</sup> mice showed reduced migration, proliferation and ECM synthesis in response to hypoxia. | 28214509 | 2017 | ||||
|
0.070 | Biomarker | disease | BEFREE | In conclusion, miR-29b plays a protective role in AngII-mediated cardiac remodeling and may be a therapeutic agent for cardiac fibrosis by targeting the TGF-β/Smad3 pathway. | 24569834 | 2014 |