E
Eiki Takimoto
Researcher at Johns Hopkins University
Publications - 62
Citations - 6119
Eiki Takimoto is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: cGMP-dependent protein kinase & Pressure overload. The author has an hindex of 33, co-authored 49 publications receiving 5602 citations. Previous affiliations of Eiki Takimoto include University of Tokyo.
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Journal ArticleDOI
Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy
Eiki Takimoto,Hunter C. Champion,Manxiang Li,Diego F. Belardi,Shuxun Ren,E. Rene Rodriguez,Djahida Bedja,Kathleen L. Gabrielson,Yibin Wang,David A. Kass +9 more
TL;DR: It is shown that blocking the intrinsic catabolism of cGMP with an oral phosphodiesterase-5A (PDE5A) inhibitor (sildenafil) suppresses chamber and myocyte hypertrophy, and improves in vivo heart function in mice exposed to chronic pressure overload induced by transverse aortic constriction.
Journal ArticleDOI
Role of Oxidative Stress in Cardiac Hypertrophy and Remodeling
Eiki Takimoto,David A. Kass +1 more
TL;DR: Recent experimental evidence for the role of oxidant stress on cardiac remodeling is discussed, focusing on pressure- overload–induced hypertrophy and dilation.
Journal ArticleDOI
Oxidant stress from nitric oxide synthase-3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load.
Eiki Takimoto,Hunter C. Champion,Manxiang Li,Shuxun Ren,E. Rene Rodriguez,E. Rene Rodriguez,Barbara Tavazzi,Giuseppe Lazzarino,Nazareno Paolocci,Kathleen L. Gabrielson,Yibin Wang,David A. Kass +11 more
TL;DR: Pressure overload triggers NOS3 uncoupling as a prominent source of myocardial ROS that contribute to dilatory remodeling and cardiac dysfunction, and reversal of this process by BH4 suggests a potential treatment to ameliorate the pathophysiology of chronic pressure-induced hypertrophy.
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Pivotal role of cardiomyocyte TGF-β signaling in the murine pathological response to sustained pressure overload
Norimichi Koitabashi,Thomas Danner,Ari L. Zaiman,Yigal M. Pinto,Janelle Rowell,Joseph L. Mankowski,Dou Zhang,Taishi Nakamura,Eiki Takimoto,David A. Kass +9 more
TL;DR: It is shown that TGF-β suppression in cardiomyocytes was required to protect against maladaptive remodeling and involved noncanonical (non-Smad-related) signaling and non canonical pathways predominantly affecting the mal Adaptive hypertrophy/dysfunction in hearts subjected to pressure overload.
Journal ArticleDOI
Phosphodiesterase 9A controls nitric-oxide-independent cGMP and hypertrophic heart disease
Dong I. Lee,Guangshuo Zhu,Takashi Sasaki,Gun Sik Cho,Nazha Hamdani,Ronald J. Holewinski,Su Hyun Jo,Thomas Danner,Manling Zhang,Peter P. Rainer,Djahida Bedja,Jonathan A. Kirk,Mark J. Ranek,Wolfgang R. Dostmann,Chulan Kwon,Kenneth B. Margulies,Jennifer E. Van Eyk,Walter Paulus,Eiki Takimoto,David A. Kass +19 more
TL;DR: It is shown that cGMP-selective PDE9A is expressed in the mammalian heart, including humans, and is upregulated by hypertrophy and cardiac failure, and its role in stress-induced heart disease suggests potential as a therapeutic target.