%0 Journal Article %1 matsushita2018chronic %A Matsushita, N. %A Ishida, N. %A Ibi, M. %A Saito, M. %A Sanbe, A. %A Shimojo, H. %A Suzuki, S. %A Koepsell, H. %A Takeishi, Y. %A Morino, Y. %A Taira, E. %A Sawa, Y. %A Hirose, M. %D 2018 %J Int Heart J %K Adrenergic Agonists/adverse Receptor alpha-1 effects myOwn %N 5 %P 1123-1133 %R 10.1536/ihj.17-565 %T Chronic Pressure Overload Induces Cardiac Hypertrophy and Fibrosis via Increases in SGLT1 and IL-18 Gene Expression in Mice %U https://www.ncbi.nlm.nih.gov/pubmed/30101852 %V 59 %X Increased gene expression levels of sodium-glucose cotransporter 1 (SGLT1) are associated with hypertrophic and ischemic cardiomyopathy. However, it remains unclear whether chronic pressure overload increases SGLT1 expression, which in turn induces hypertrophic cardiomyopathy. We hypothesized that pressure overload could increase SGLT1 gene expression, leading to the development of hypertrophic cardiomyopathy.To create pressure overload-induced cardiomyopathy, transverse aortic constriction (TAC) was performed in SGLT1-deficient (SGLT1(-/-)) and wild-type (WT) mice. Six weeks after surgery, all mice were investigated. We observed a reduction of left ventricular fractional shortening and left ventricular dilatation in TAC-operated WT but not in TAC-operated SGLT1(-/-) mice. SGLT1, interleukin 18, connective tissue growth factor, and collagen type 1 gene expression levels were increased in TAC-operated WT mouse hearts compared with that of sham-operated WT mouse hearts. Moreover, heart/body weight ratio and ventricular interstitial fibrosis were increased in TAC-operated WT mice compared with that of sham-operated WT mice. Interestingly, these factors did not increase in TAC-operated SGLT1(-/-) mice compared with that of sham-operated WT and SGLT1(-/-) mice. Phenylephrine, an adrenergic alpha(1) receptor agonist, caused cardiomyocyte hypertrophy in neonatal WT mouse hearts to a significantly larger extent than in neonatal SGLT1(-/-) mouse hearts.In conclusion, the results indicate that chronic pressure overload increases SGLT1 and IL-18 gene expressions, leading to the development of hypertrophic cardiomyopathy. These results make SGLT1 a potential candidate for the therapeutic target for hypertension-induced cardiomyopathy.

@article{matsushita2018chronic, abstract = {Increased gene expression levels of sodium-glucose cotransporter 1 (SGLT1) are associated with hypertrophic and ischemic cardiomyopathy. However, it remains unclear whether chronic pressure overload increases SGLT1 expression, which in turn induces hypertrophic cardiomyopathy. We hypothesized that pressure overload could increase SGLT1 gene expression, leading to the development of hypertrophic cardiomyopathy.To create pressure overload-induced cardiomyopathy, transverse aortic constriction (TAC) was performed in SGLT1-deficient (SGLT1(-/-)) and wild-type (WT) mice. Six weeks after surgery, all mice were investigated. We observed a reduction of left ventricular fractional shortening and left ventricular dilatation in TAC-operated WT but not in TAC-operated SGLT1(-/-) mice. SGLT1, interleukin 18, connective tissue growth factor, and collagen type 1 gene expression levels were increased in TAC-operated WT mouse hearts compared with that of sham-operated WT mouse hearts. Moreover, heart/body weight ratio and ventricular interstitial fibrosis were increased in TAC-operated WT mice compared with that of sham-operated WT mice. Interestingly, these factors did not increase in TAC-operated SGLT1(-/-) mice compared with that of sham-operated WT and SGLT1(-/-) mice. Phenylephrine, an adrenergic alpha(1) receptor agonist, caused cardiomyocyte hypertrophy in neonatal WT mouse hearts to a significantly larger extent than in neonatal SGLT1(-/-) mouse hearts.In conclusion, the results indicate that chronic pressure overload increases SGLT1 and IL-18 gene expressions, leading to the development of hypertrophic cardiomyopathy. These results make SGLT1 a potential candidate for the therapeutic target for hypertension-induced cardiomyopathy.}, added-at = {2024-02-15T15:08:22.000+0100}, author = {Matsushita, N. and Ishida, N. and Ibi, M. and Saito, M. and Sanbe, A. and Shimojo, H. and Suzuki, S. and Koepsell, H. and Takeishi, Y. and Morino, Y. and Taira, E. and Sawa, Y. and Hirose, M.}, biburl = {https://www.bibsonomy.org/bibtex/2d2b4a263183c992d8c7dda3ac7cbba3a/jvsi_all}, doi = {10.1536/ihj.17-565}, interhash = {531e3a7bd0263ce7a0391611c2163e73}, intrahash = {d2b4a263183c992d8c7dda3ac7cbba3a}, issn = {1349-3299 (Electronic) 1349-2365 (Linking)}, journal = {Int Heart J}, keywords = {Adrenergic Agonists/adverse Receptor alpha-1 effects myOwn}, note = {Matsushita, Naoko Ishida, Nanae Ibi, Miho Saito, Maki Sanbe, Atsushi Shimojo, Hisashi Suzuki, Satoshi Koepsell, Hermann Takeishi, Yasuchika Morino, Yoshihiro Taira, Eiichi Sawa, Yohei Hirose, Masamichi eng Comparative Study Japan 2018/08/14 Int Heart J. 2018 Sep 26;59(5):1123-1133. doi: 10.1536/ihj.17-565. Epub 2018 Aug 11.}, number = 5, pages = {1123-1133}, timestamp = {2024-02-15T15:08:22.000+0100}, title = {Chronic Pressure Overload Induces Cardiac Hypertrophy and Fibrosis via Increases in SGLT1 and IL-18 Gene Expression in Mice}, type = {Journal Article}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30101852}, volume = 59, year = 2018 }