Involvement of PARK2-Mediated Mitophagy in Idiopathic Pulmonary Fibrosis Pathogenesis.

@article{Kobayashi2016InvolvementOP,
  title={Involvement of PARK2-Mediated Mitophagy in Idiopathic Pulmonary Fibrosis Pathogenesis.},
  author={Kenji Kobayashi and Jun Araya and Shunsuke Minagawa and Hiromichi Hara and Nayuta Saito and Tsukasa Kadota and Nahoko Sato and Masahiro Yoshida and Kazuya Tsubouchi and Yusuke Kurita and Saburo Ito and Yu Fujita and Naoki Takasaka and Hirofumi Utsumi and Haruhiko Yanagisawa and Mitsuo Hashimoto and Hiroshi Wakui and Jun ichi Kojima and Kenichiro Shimizu and Takanori Numata and Makoto Kawaishi and Yumi Kaneko and Hisatoshi Asano and Makoto Yamashita and Makoto Odaka and Toshiaki Morikawa and Katsutoshi Nakayama and Kazuyoshi Kuwano},
  journal={Journal of immunology},
  year={2016},
  volume={197 2},
  pages={504-16}
}
Fibroblastic foci, known to be the leading edge of fibrosis development in idiopathic pulmonary fibrosis (IPF), are composed of fibrogenic myofibroblasts. Autophagy has been implicated in the regulation of myofibroblast differentiation. Insufficient mitophagy, the mitochondria-selective autophagy, results in increased reactive oxygen species, which may modulate cell signaling pathways for myofibroblast differentiation. Therefore, we sought to investigate the regulatory role of mitophagy in… CONTINUE READING
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