S
Shouji Matsushima
Researcher at Kyushu University
Publications - 111
Citations - 5875
Shouji Matsushima is an academic researcher from Kyushu University. The author has contributed to research in topics: Heart failure & Medicine. The author has an hindex of 31, co-authored 87 publications receiving 4656 citations. Previous affiliations of Shouji Matsushima include Hokkaido University & Rutgers University.
Papers
More filters
Journal ArticleDOI
Oxidative stress and heart failure
TL;DR: Oxidative stress is involved in the pathophysiology of HF in the heart as well as in the skeletal muscle, and a better understanding of these mechanisms may enable the development of novel and effective therapeutic strategies against HF.
Journal ArticleDOI
NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
Junya Kuroda,Tetsuro Ago,Shouji Matsushima,Peiyong Zhai,Michael D. Schneider,Junichi Sadoshima +5 more
TL;DR: It is suggested that Nox4 in cardiac myocytes is a major source of mitochondrial oxidative stress, thereby mediating mitochondrial and cardiac dysfunction during PO.
Journal ArticleDOI
Silent Information Regulator 1 Protects the Heart From Ischemia/Reperfusion
Chiao Po Hsu,Peiyong Zhai,Takanobu Yamamoto,Yasuhiro Maejima,Shouji Matsushima,Nirmala Hariharan,Dan Shao,Hiromitsu Takagi,Shinichi Oka,Junichi Sadoshima +9 more
TL;DR: In this article, the authors examined whether Sirt1 is protective against myocardial ischemia/reperfusion (I/R) in transgenic mice with cardiac-specific overexpression.
Journal ArticleDOI
Mitochondrial oxidative stress and dysfunction in myocardial remodelling.
TL;DR: Overexpression of the genes for peroxiredoxin-3 (Prx-3), a mitochondrial antioxidant, or mitochondrial transcription factor A (TFAM), could ameliorate the decline in mtDNA copy number in failing hearts and inhibit the decrease in mitochondrial function.
Journal ArticleDOI
Inhibition of TGF-β signaling exacerbates early cardiac dysfunction but prevents late remodeling after infarction
Masaki Ikeuchi,Hiroyuki Tsutsui,Tetsuya Shiomi,Hidenori Matsusaka,Shouji Matsushima,Jing Wen,Toru Kubota,Akira Takeshita +7 more
TL;DR: The activation of TGF-beta is protective against ischemic myocardial damage during the early phase, however, the beneficial effects might be lost, when its expression is sustained, thereby leading to LV remodeling and failure after MI.