| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10953830 | Journal of Molecular and Cellular Cardiology | 2012 | 10 Pages |
Abstract
⺠p53 was activated and damaged mitochondria were accumulated in ischemic myocardium. ⺠We found TIGAR was up-regulated by ischemic injury. ⺠TIGAR inhibited myocyte mitophagy by inactivating ROS signal to Bnip3. ⺠Accumulation of damaged mitochondria and cell death resulted in cardiac dysfunction. ⺠Dysregulation of mitochondrial quality by p53/TIGAR is a novel therapeutic target.
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Authors
Atsushi Hoshino, Satoaki Matoba, Eri Iwai-Kanai, Hideo Nakamura, Masaki Kimata, Mikihiko Nakaoka, Maki Katamura, Yoshifumi Okawa, Makoto Ariyoshi, Yuichiro Mita, Koji Ikeda, Tomomi Ueyama, Mitsuhiko Okigaki, Hiroaki Matsubara,