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Novel mechanism of cardiac protection by valsartan: synergetic roles of TGF-β1 and HIF-1α in Ang II-mediated fibrosis after myocardial infarction.

Sui X, Wei H, Wang D - J. Cell. Mol. Med. (2015)

Bottom Line: By blocking with valsartan, a blocker of Ang II type I (AT1) receptor, we confirmed that the up-regulation of TGF-β/Smad and Hif-1α was through the Ang II-mediated pathway.By administering TGF-β or dimethyloxalylglycine, we determined that both TGF-β/Smad and Hif-1α contributed to Ang II-mediated collagen accumulation and a synergetic effect between them was observed.Heart function, infarcted size, wall thickness as well as myocardial vascularization of ischaemic hearts were also significantly improved by valsartan compared with saline and hydralazine.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiothoracic Surgery, The Civil Aviation General Hospital, Chaoyang District, Beijing, China.

No MeSH data available.


Related in: MedlinePlus

Influence of valsartan on myocardial expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins 1 week after MI. Compared with animals of MI, administering valsartan significantly decreased the expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins (MMP-2 and MMP-9) which were up-regulated after MI. Ischaemia indicates animals with MI and receiving saline treatment. Valsartan indicates animals receiving valsartan treatment (n = 5).
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fig03: Influence of valsartan on myocardial expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins 1 week after MI. Compared with animals of MI, administering valsartan significantly decreased the expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins (MMP-2 and MMP-9) which were up-regulated after MI. Ischaemia indicates animals with MI and receiving saline treatment. Valsartan indicates animals receiving valsartan treatment (n = 5).

Mentions: To validate the cardiac protective effects of valsartan after ischaemia, a rat model of MI was prepared and valsartan was administered. At 1 week, hearts were explanted and Western blotting was performed. As shown in Figure3, TGF-β1/Smad and HIF-1α pathways were up-regulated after MI, but they were significantly suppressed by the administration of valsartan. MI-induced up-regulation of fibrosis-related proteins; MMP2 and MMP9 were also suppressed by valsartan, indicating that valsartan may attenuate myocardial fibrosis after MI, consistent with in vitro results.


Novel mechanism of cardiac protection by valsartan: synergetic roles of TGF-β1 and HIF-1α in Ang II-mediated fibrosis after myocardial infarction.

Sui X, Wei H, Wang D - J. Cell. Mol. Med. (2015)

Influence of valsartan on myocardial expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins 1 week after MI. Compared with animals of MI, administering valsartan significantly decreased the expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins (MMP-2 and MMP-9) which were up-regulated after MI. Ischaemia indicates animals with MI and receiving saline treatment. Valsartan indicates animals receiving valsartan treatment (n = 5).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549028&req=5

fig03: Influence of valsartan on myocardial expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins 1 week after MI. Compared with animals of MI, administering valsartan significantly decreased the expression of TGF-1β/Smad, Hif-1α and fibrosis-related proteins (MMP-2 and MMP-9) which were up-regulated after MI. Ischaemia indicates animals with MI and receiving saline treatment. Valsartan indicates animals receiving valsartan treatment (n = 5).
Mentions: To validate the cardiac protective effects of valsartan after ischaemia, a rat model of MI was prepared and valsartan was administered. At 1 week, hearts were explanted and Western blotting was performed. As shown in Figure3, TGF-β1/Smad and HIF-1α pathways were up-regulated after MI, but they were significantly suppressed by the administration of valsartan. MI-induced up-regulation of fibrosis-related proteins; MMP2 and MMP9 were also suppressed by valsartan, indicating that valsartan may attenuate myocardial fibrosis after MI, consistent with in vitro results.

Bottom Line: By blocking with valsartan, a blocker of Ang II type I (AT1) receptor, we confirmed that the up-regulation of TGF-β/Smad and Hif-1α was through the Ang II-mediated pathway.By administering TGF-β or dimethyloxalylglycine, we determined that both TGF-β/Smad and Hif-1α contributed to Ang II-mediated collagen accumulation and a synergetic effect between them was observed.Heart function, infarcted size, wall thickness as well as myocardial vascularization of ischaemic hearts were also significantly improved by valsartan compared with saline and hydralazine.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiothoracic Surgery, The Civil Aviation General Hospital, Chaoyang District, Beijing, China.

No MeSH data available.


Related in: MedlinePlus