What question did this study set out to answer?

To investigate the molecular mechanisms regulating periostin expression in cardiac cells exposed to angiotensin II and mechanical stretch, and to assess whether valsartan attenuates periostin-mediated remodeling after myocardial infarction.

May 8, 2007Hypertension

Novel Mechanisms of Valsartan on the Treatment of Acute Myocardial Infarction Through Inhibition of the Antiadhesion Molecule Periostin

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Authors

KIKazuma IekushiNovartis (Japan)YTYoshiaki TaniyamaThe University of Osaka JAJunya AzumaMorinomiya University of Medical Sciences

Discussion

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Overview

Does not support changing post-MI valsartan use; leaves open periostin as a remodeling target for future therapies.

Key Points

To investigate the molecular mechanisms regulating periostin expression in cardiac cells exposed to angiotensin II and mechanical stretch, and to assess whether valsartan attenuates periostin-mediated remodeling after myocardial infarction.
Assessed periostin expression in cultured cardiac myocytes and fibroblasts treated with angiotensin II, kinase pathway inhibitors, mechanical stretch, valsartan, and neutralizing antibodies.
Evaluated in vivo myocardial periostin levels and cardiac function at 4 weeks post-myocardial infarction with and without valsartan therapy.
Angiotensin II significantly upregulated periostin in myocytes and fibroblasts via PI3K, JNK, p38, and ERK1/2 pathways (P<0.05).
Mechanical stretch significantly elevated periostin expression (P<0.05), which was partially inhibited by valsartan and nearly completely abolished by valsartan combined with TGF-β and PDGF-BB neutralizing antibodies (P<0.05).
Periostin expression rose significantly in infarcted myocardium (P<0.05), whereas 4-week valsartan treatment significantly attenuated periostin upregulation and improved cardiac dysfunction (P<0.05).

Cite This Study

Iekushi et al. (2007) studied this question.

synapsesocial.com/papers/6a74155c55a91aadd1391b2c https://doi.org/10.1161/hypertensionaha.106.080994

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May 8, 2007Hypertension

Novel Mechanisms of Valsartan on the Treatment of Acute Myocardial Infarction Through Inhibition of the Antiadhesion Molecule Periostin

View Full Paper

Ask AI

Bookmark

Authors

KIKazuma IekushiNovartis (Japan)YTYoshiaki TaniyamaThe University of Osaka JAJunya AzumaMorinomiya University of Medical Sciences

Discussion

Member takes

Overview

Does not support changing post-MI valsartan use; leaves open periostin as a remodeling target for future therapies.

Key Points

To investigate the molecular mechanisms regulating periostin expression in cardiac cells exposed to angiotensin II and mechanical stretch, and to assess whether valsartan attenuates periostin-mediated remodeling after myocardial infarction.
Assessed periostin expression in cultured cardiac myocytes and fibroblasts treated with angiotensin II, kinase pathway inhibitors, mechanical stretch, valsartan, and neutralizing antibodies.
Evaluated in vivo myocardial periostin levels and cardiac function at 4 weeks post-myocardial infarction with and without valsartan therapy.
Angiotensin II significantly upregulated periostin in myocytes and fibroblasts via PI3K, JNK, p38, and ERK1/2 pathways (P<0.05).
Mechanical stretch significantly elevated periostin expression (P<0.05), which was partially inhibited by valsartan and nearly completely abolished by valsartan combined with TGF-β and PDGF-BB neutralizing antibodies (P<0.05).
Periostin expression rose significantly in infarcted myocardium (P<0.05), whereas 4-week valsartan treatment significantly attenuated periostin upregulation and improved cardiac dysfunction (P<0.05).

Cite This Study

Iekushi et al. (2007) studied this question.

synapsesocial.com/papers/6a74155c55a91aadd1391b2c https://doi.org/10.1161/hypertensionaha.106.080994

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