Involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis

Altered iron homeostasis resulting in excessive oxidative stress has been implicated in smoke-induced lung diseases. Here the authors show that ferroptosis of lung epithelial cells, potentially resulting from excessive ferritinophagy, is involved in the pathogenesis of COPD.

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Detalles Bibliográficos
Autores principales: Masahiro Yoshida, Shunsuke Minagawa, Jun Araya, Taro Sakamoto, Hiromichi Hara, Kazuya Tsubouchi, Yusuke Hosaka, Akihiro Ichikawa, Nayuta Saito, Tsukasa Kadota, Nahoko Sato, Yusuke Kurita, Kenji Kobayashi, Saburo Ito, Hirohumi Utsumi, Hiroshi Wakui, Takanori Numata, Yumi Kaneko, Shohei Mori, Hisatoshi Asano, Makoto Yamashita, Makoto Odaka, Toshiaki Morikawa, Katsutoshi Nakayama, Takeo Iwamoto, Hirotaka Imai, Kazuyoshi Kuwano
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/7f973dabdbee4e05bfa82fda5c334da7
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Sumario:Altered iron homeostasis resulting in excessive oxidative stress has been implicated in smoke-induced lung diseases. Here the authors show that ferroptosis of lung epithelial cells, potentially resulting from excessive ferritinophagy, is involved in the pathogenesis of COPD.