Zobrazeno 1 - 10
of 29
pro vyhledávání: '"Naoko Matsushita"'
Autor:
Yohei Sawa, Maki Saito, Nanae Ishida, Miho Ibi, Naoko Matsushita, Yoshihiro Morino, Eiichi Taira, Masamichi Hirose
Publikováno v:
Journal of Pharmacological Sciences, Vol 142, Iss 1, Pp 16-25 (2020)
Recent studies demonstrated that sodium-glucose co-transporter 1 (SGLT1) is associated with human ischemic cardiomyopathy. However, whether SGLT1 blockade is effective against ischemic cardiomyopathy is still uncertain. We examined the effects of KGA
Externí odkaz:
https://doaj.org/article/8781f89ea6d64226b12dd58104ca0221
Autor:
Naoko Matsushita, Toshihide Kashihara, Hisashi Shimojo, Satoshi Suzuki, Tsutomu Nakada, Yasuchika Takeishi, Ulrike Mende, Eiichi Taira, Mitsuhiko Yamada, Atsushi Sanbe, Masamichi Hirose
Publikováno v:
PLoS ONE, Vol 9, Iss 8, p e106354 (2014)
Transgenic mice with transient cardiac expression of constitutively active Galpha q (Gαq-TG) exhibt progressive heart failure and ventricular arrhythmias after the initiating stimulus of transfected constitutively active Gαq becomes undetectable. H
Externí odkaz:
https://doaj.org/article/645fbbeae7b649299460c15e1a616d18
Autor:
Masamichi Hirose, Yasuchika Takeishi, Tsutomu Nakada, Hisashi Shimojo, Toshihide Kashihara, Ayako Nishio, Satoshi Suzuki, Ulrike Mende, Kiyoshi Matsumoto, Naoko Matsushita, Eiichi Taira, Fumika Sato, Mitsuhiko Yamada
Publikováno v:
PLoS ONE, Vol 7, Iss 12, p e52667 (2012)
BACKGROUND: Beneficial effects of nicorandil on the treatment of hypertensive heart failure (HF) and ischemic heart disease have been suggested. However, whether nicorandil has inhibitory effects on HF and ventricular arrhythmias caused by the activa
Externí odkaz:
https://doaj.org/article/9a75165fd9364367903c0befe0366274
Autor:
Atsushi, Sanbe, Yui, Inomata, Naoko, Matsushita, Yohei, Sawa, Chizuru, Hino, Hinano, Yamazaki, Kei, Takanohashi, Natsuko, Takahashi, Rieko, Higashio, Hideki, Tsumura, Toshinori, Aoyagi, Masamichi, Hirose
Publikováno v:
Biochemical and Biophysical Research Communications. 631:48-54
Histone deacetylase 6 (HDAC6) is known to deacetylate amino acid lysine in alpha-tubulin. However, the functional role of HDAC6 in the progression of cardiac disease remains uncertain. The functional role of HDAC6 in the hearts was examined using tra
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1bf96136e55d3ae08defbe82243b1ae4
https://doi.org/10.1016/j.bbrc.2022.09.055
https://doi.org/10.1016/j.bbrc.2022.09.055
Autor:
Zhenghua Li, Hideki Kanazashi, Yoshimi Tokashiki, Rie Fujikawa, Ayaka Okagaki, Sho Katoh, Kenta Kojima, Kyoko Haruna, Naoko Matsushita, Tomo-o Ishikawa, Hong Chen, Kenichi Yamamura
Publikováno v:
Biochemical and Biophysical Research Communications. 599:69-74
Familial amyloidotic polyneuropathy (FAP) is caused by a mutation in the transthyretin (TTR) gene. In addition, deposition of wild-type TTR can cause senile systemic amyloidosis (SSA). To date, we have produced several transgenic mouse models for FAP
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6972d571e8dc2586ef319dc6ccf9adbc
https://doi.org/10.1016/j.bbrc.2022.02.035
https://doi.org/10.1016/j.bbrc.2022.02.035
Autor:
Masamichi Hirose, Maki Saito, Naoko Matsushita, Miho Ibi, Eiichi Taira, Yoshihiro Morino, Yohei Sawa, Nanae Ishida
Publikováno v:
Journal of Pharmacological Sciences, Vol 142, Iss 1, Pp 16-25 (2020)
Recent studies demonstrated that sodium-glucose co-transporter 1 (SGLT1) is associated with human ischemic cardiomyopathy. However, whether SGLT1 blockade is effective against ischemic cardiomyopathy is still uncertain. We examined the effects of KGA
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::70f9b5aad4cfd8ae0297c31b2334f81e
http://www.sciencedirect.com/science/article/pii/S1347861319357263
http://www.sciencedirect.com/science/article/pii/S1347861319357263
Autor:
Miho Ibi, Nanae Ishida, Yoshihiro Morino, Yohei Sawa, Masamichi Hirose, Eiichi Taira, Masafumi Takahashi, Maki Saito, Yoichiro Iwakura, Shun'ichiro Taniguchi, Naoko Matsushita
Publikováno v:
Biological and Pharmaceutical Bulletin. 42:543-546
Hypertension is one risk for atrial fibrillation (AF) and induces cardiac inflammation. Recent evidence indicates that pressure overload-induced ventricular structural remodeling is associated with the activation of nucleotide binding-oligomerization
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::939760bb5b54dbe329b0c0c07b8cf90b
https://doi.org/10.1248/bpb.b18-00363
https://doi.org/10.1248/bpb.b18-00363
Autor:
Atsushi Sanbe, Yui Inomata, Yohei Sawa, Naoko Matsushita, Nanae Ishida, Rieko Higashio, Masamichi Hirose
Publikováno v:
Proceedings for Annual Meeting of The Japanese Pharmacological Society. 95:1
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::2f5dfcec07ae89e5f763c3095a6b1655
https://doi.org/10.1254/jpssuppl.95.0_1-p-044
https://doi.org/10.1254/jpssuppl.95.0_1-p-044
Autor:
Nanae Ishida, Hermann Koepsell, Eiichi Taira, Yasuchika Takeishi, Yohei Sawa, Naoko Matsushita, Satoshi Suzuki, Hisashi Shimojo, Miho Ibi, Maki Saito, Masamichi Hirose, Atsushi Sanbe, Yoshihiro Morino
Publikováno v:
International Heart Journal. 59:1123-1133
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 h
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::9bcc558decb285a9f462aa258cadecdb
https://doi.org/10.1536/ihj.17-565
https://doi.org/10.1536/ihj.17-565
Publikováno v:
Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan. 138(7)
It is well-known that metabolic remodeling occurs in the presence of cardiomyopathy induced by cardiac ischemia and hypertrophy, and diabetes mellitus. It is also known that a novel cardiac glucose transporter, sodium-glucose co-transporter 1 (SGLT1)
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4359f57c732cca948006f4fce8b1c66c
https://pubmed.ncbi.nlm.nih.gov/29962473
https://pubmed.ncbi.nlm.nih.gov/29962473