Literature DB >> 12899937

Pathways of cell signaling in hyperoxia.

Patty J Lee1, Augustine M K Choi.   

Abstract

Administration of high concentrations of oxygen (hyperoxia) is a mainstay of supportive treatment for patients suffering from severe respiratory failure. However, hyperoxia, by generating excess systemic reactive oxygen species (ROS), can exacerbate organ failure by causing cellular injury. Therefore, a better understanding of the signal transduction pathways in hyperoxia may provide the basis for effective therapeutic interventions. The major biological effects of hyperoxia include cell death, induction of stress responses, inflammation, and modulation of cell growth. Major signaling pathways that appear to be involved include the mitogen-activated protein kinases (MAPKs), AP-1, and NF-kappa B, which converge, ultimately, to the expression of a range of stress response genes, cytokines, and growth factors.

Entities:  

Mesh:

Substances:

Year:  2003        PMID: 12899937     DOI: 10.1016/s0891-5849(03)00279-x

Source DB:  PubMed          Journal:  Free Radic Biol Med        ISSN: 0891-5849            Impact factor:   7.376


  57 in total

1.  TLR signaling prevents hyperoxia-induced lung injury by protecting the alveolar epithelium from oxidant-mediated death.

Authors:  Megan N Ballinger; Michael W Newstead; Xianying Zeng; Urvashi Bhan; Jeffrey C Horowitz; Bethany B Moore; David J Pinsky; Richard A Flavell; Theodore J Standiford
Journal:  J Immunol       Date:  2012-06-01       Impact factor: 5.422

2.  Formation of ternary complex of human biliverdin reductase-protein kinase Cδ-ERK2 protein is essential for ERK2-mediated activation of Elk1 protein, nuclear factor-κB, and inducible nitric-oxidase synthase (iNOS).

Authors:  Peter E M Gibbs; Tihomir Miralem; Nicole Lerner-Marmarosh; Cicerone Tudor; Mahin D Maines
Journal:  J Biol Chem       Date:  2011-11-07       Impact factor: 5.157

3.  MCP-1/CCR2 signalling pathway regulates hyperoxia-induced acute lung injury via nitric oxide production.

Authors:  Toshiyuki Okuma; Yasuhiro Terasaki; Naomi Sakashita; Koichi Kaikita; Hironori Kobayashi; Takanori Hayasaki; William A Kuziel; Hideo Baba; Motohiro Takeya
Journal:  Int J Exp Pathol       Date:  2006-12       Impact factor: 1.925

4.  Preparation and preservation of hypoxia UW solution.

Authors:  Chidang Wan; Chunyou Wang; Tao Liu; Rui Cheng; Zhiyong Yang
Journal:  J Huazhong Univ Sci Technolog Med Sci       Date:  2007-10

5.  Dual oxidase 2 in lung epithelia is essential for hyperoxia-induced acute lung injury in mice.

Authors:  Min-Ji Kim; Jae-Chan Ryu; Younghee Kwon; Suhee Lee; Yun Soo Bae; Joo-Heon Yoon; Ji-Hwan Ryu
Journal:  Antioxid Redox Signal       Date:  2014-06-26       Impact factor: 8.401

6.  Exercise and diet-induced weight loss attenuates oxidative stress related-coronary vasoconstriction in obese adolescents.

Authors:  Zhaohui Gao; Marsha Novick; Matthew D Muller; Ronald J Williams; Samson Spilk; Urs A Leuenberger; Lawrence I Sinoway
Journal:  Eur J Appl Physiol       Date:  2012-07-20       Impact factor: 3.078

7.  Ageing and genetic background influence anaesthetic effects in a D. melanogaster model of blunt trauma with brain injury.

Authors:  Hannah J Schiffman; Zachariah P G Olufs; Michael R Lasarev; David A Wassarman; Misha Perouansky
Journal:  Br J Anaesth       Date:  2020-05-25       Impact factor: 9.166

8.  Experimental study on the cryopreservation of LLC-PK1 epithelial cells with hypoxic UW solution.

Authors:  Chidan Wan; Chunyou Wang; Tao Liu; Hongbo Wang; Zhiyong Yang
Journal:  J Huazhong Univ Sci Technolog Med Sci       Date:  2007-08

9.  Experimental selection for Drosophila survival in extremely high O2 environments.

Authors:  Huiwen W Zhao; Dan Zhou; Victor Nizet; Gabriel G Haddad
Journal:  PLoS One       Date:  2010-07-23       Impact factor: 3.240

Review 10.  The antioxidant response element and oxidative stress modifiers in airway diseases.

Authors:  Sekhar P Reddy
Journal:  Curr Mol Med       Date:  2008-08       Impact factor: 2.222

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.