z-logo
open-access-imgOpen Access
Endogenous Hydrogen Sulfide Ameliorates NOX4 Induced Oxidative Stress in LPS-Stimulated Macrophages and Mice
Author(s) -
Xiling Wang,
LiLong Pan,
Fen Long,
Weijun Wu,
Di Yan,
Peng Xu,
Siyu Liu,
Ming Qin,
Wanwan Jia,
Xinhua Liu,
Yi Zhun Zhu
Publication year - 2018
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000489980
Subject(s) - nox4 , nadph oxidase , oxidative stress , inflammation , protein kinase b , lipopolysaccharide , knockout mouse , gene knockdown , pi3k/akt/mtor pathway , chemistry , signal transduction , reactive oxygen species , biology , microbiology and biotechnology , immunology , biochemistry , apoptosis , receptor
Sepsis is a severe and complicated syndrome that is characterized by dysregulation of host inflammatory responses and organ failure. Cystathionine-γ-lyase (CSE)/ hydrogen sulfide (H2S) has potential anti-inflammatory activities in a variety of inflammatory diseases. NADPH oxidase 4 (Nox4), a member of the NADPH oxidases, is the major source of reactive oxygen species (ROS) and its expression is increased in sepsis, but its function in CSE-mediated anti-inflammatory activities remains unknown.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom