S
Shoji Sanada
Researcher at Osaka University
Publications - 12
Citations - 1683
Shoji Sanada is an academic researcher from Osaka University. The author has contributed to research in topics: Vasodilation & Muscle hypertrophy. The author has an hindex of 11, co-authored 12 publications receiving 1539 citations. Previous affiliations of Shoji Sanada include Brigham and Women's Hospital.
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Journal ArticleDOI
IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system
Shoji Sanada,Daihiko Hakuno,Luke J. Higgins,Eric R. Schreiter,Andrew Neil James Mckenzie,Richard T. Lee +5 more
TL;DR: IL-33/ST2 signaling is a mechanically activated, cardioprotective fibroblast-cardiomyocyte paracrine system, which is believed to be novel and may have therapeutic potential for beneficially regulating the myocardial response to overload.
Journal ArticleDOI
Interleukin-33 Prevents Apoptosis and Improves Survival After Experimental Myocardial Infarction Through ST2 Signaling
Kenjiro Seki,Shoji Sanada,Anastacia Y. Kudinova,Matthew L. Steinhauser,Vandna Handa,Joseph Gannon,Richard T. Lee +6 more
TL;DR: IL-33 prevents cardiomyocyte apoptosis and improves cardiac function and survival after MI through ST2 signaling and both echocardiographic and hemodynamic studies revealed that IL-33 improved ventricular function.
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Protein Kinase A as Another Mediator of Ischemic Preconditioning Independent of Protein Kinase C
Shoji Sanada,Hiroshi Asanuma,Osamu Tsukamoto,Tetsuo Minamino,Koichi Node,Seiji Takashima,Tomi Fukushima,Akiko Ogai,Yoshiro Shinozaki,Masashi Fujita,Akio Hirata,Hiroko Okuda,Hiroaki Shimokawa,Hitonobu Tomoike,Masatsugu Hori,Masafumi Kitakaze +15 more
TL;DR: Transient preischemic activation of PKA reduces infarct size through Rho-kinase inhibition and actin cytoskeletal deactivation during sustained ischemia, implicating a novel mechanism for cardioprotection by ischemic preconditioning independent of PKC and a potential new therapeutic target.
Journal ArticleDOI
Optimal Windows of Statin Use for Immediate Infarct Limitation 5-Nucleotidase as Another Downstream Molecule of Phosphatidylinositol 3-Kinase
Shoji Sanada,Hiroshi Asanuma,Tetsuo Minamino,Koichi Node,Seiji Takashima,Hiroko Okuda,Yoshiro Shinozaki,Akiko Ogai,Masashi Fujita,Akio Hirata,Jiyoong Kim,Yoshihiro Asano,Hidezo Mori,Hitonobu Tomoike,Soichiro Kitamura,Masatsugu Hori,Masafumi Kitakaze +16 more
TL;DR: In this paper, the authors investigated the effect of statins on ischemic-reperfusion injury and the underlying mechanisms of such effects in an in vivo canine model, and they found that myocardial phosphatidylinositol 3-kinase (PI3-K) and 5′-nucleotidase activities were measured.
Journal ArticleDOI
Opening of Ca2+-activated K+ channels is involved in ischemic preconditioning in canine hearts.
Yasunori Shintani,Koichi Node,Hiroshi Asanuma,Shoji Sanada,Seiji Takashima,Yoshihiro Asano,Yulin Liao,Masashi Fujita,Akio Hirata,Yoshiro Shinozaki,Tomi Fukushima,Yoko Nagamachi,Hiroko Okuda,Jiyoong Kim,Hitonobu Tomoike,Masatsugu Hori,Masafumi Kitakaze +16 more
TL;DR: The opening of K(Ca) channel is involved in early trigger phase of the molecular mechanism of IP, and the cardioprotective effect of IP was not blunted by the treatment with ChTX when treated only during reperfusion.