S
Shinichi Hirotani
Researcher at Rutgers University
Publications - 4
Citations - 682
Shinichi Hirotani is an academic researcher from Rutgers University. The author has contributed to research in topics: Muscle hypertrophy & GSK3B. The author has an hindex of 4, co-authored 4 publications receiving 642 citations.
Papers
More filters
Journal ArticleDOI
Type 5 Adenylyl Cyclase Disruption Increases Longevity and Protects Against Stress
Lin Yan,Dorothy E. Vatner,J. Patrick O'Connor,Andreas S. Ivessa,Hui Ge,Wei Chen,Shinichi Hirotani,Yoshihiro Ishikawa,Junichi Sadoshima,Stephen F. Vatner +9 more
TL;DR: A significant activation of the Raf/MEK/ERK signaling pathway and upregulation of cell protective molecules, including superoxide dismutase are demonstrated and suggest that AC is a fundamentally important mechanism regulating lifespan and stress resistance.
Journal ArticleDOI
AMPK mediates autophagy during myocardial ischemia in vivo.
Hiromitsu Takagi,Yutaka Matsui,Shinichi Hirotani,Hideyuki Sakoda,Tomoichiro Asano,Junichi Sadoshima +5 more
TL;DR: The role of AMPK in mediating autophagy during myocardial ischemia in vivo and the roles of AMP-Activated Protein Kinase and Beclin 1 in Mediating Autophagy are discussed.
Journal ArticleDOI
Inhibition of Glycogen Synthase Kinase 3β During Heart Failure Is Protective
Shinichi Hirotani,Peiyong Zhai,Hideharu Tomita,Jonathan Galeotti,Juan Pablo Marquez,Shumin Gao,Chull Hong,Atsuko Yatani,Jesús Avila,Junichi Sadoshima +9 more
TL;DR: It is suggested that persistent inhibition of GSK-3&bgr; induces compensatory hypertrophy, inhibits apoptosis and fibrosis, and increases cardiac contractility and that the antiapoptotic effect of G SK-3 &b gr; inhibition is mediated by myeloid cell leukemia-1.
Journal ArticleDOI
Developmental changes in gene expression of Epac and its upregulation in myocardial hypertrophy.
Coskun Ulucan,Xu Wang,Erdene Baljinnyam,Yunzhe Bai,Satoshi Okumura,Motohiko Sato,Susumu Minamisawa,Shinichi Hirotani,Yoshihiro Ishikawa +8 more
TL;DR: Epac gene expression was upregulated in myocardial hypertrophy induced by chronic isoproterenol infusion or pressure overload by transverse aortic banding and Epac stimulation led to the activation of ERK1/2, suggesting the functional involvement of Epac in organogenesis and also in physiological as well as pathophysiological processes, such as cardiachypertrophy.