Repression of hypoxia-inducible factor-1 contributes to increased mitochondrial reactive oxygen spec...
Repression of hypoxia-inducible factor-1 contributes to increased mitochondrial reactive oxygen species production in diabetes
About this item
Full title
Author / Creator
Zheng, Xiaowei , Narayanan, Sampath , Xu, Cheng , Eliasson Angelstig, Sofie , Grünler, Jacob , Zhao, Allan , Di Toro, Alessandro , Bernardi, Luciano , Mazzone, Massimiliano , Carmeliet, Peter , Del Sole, Marianna , Solaini, Giancarlo , Forsberg, Elisabete A , Zhang, Ao , Brismar, Kerstin , Schiffer, Tomas A , Rajamand Ekberg, Neda , Botusan, Ileana Ruxandra , Palm, Fredrik and Catrina, Sergiu-Bogdan
Publisher
England: eLife Science Publications, Ltd
Journal title
Language
English
Formats
Publication information
Publisher
England: eLife Science Publications, Ltd
Subjects
More information
Scope and Contents
Contents
Excessive production of mitochondrial reactive oxygen species (ROS) is a central mechanism for the development of diabetes complications. Recently, hypoxia has been identified to play an additional pathogenic role in diabetes. In this study, we hypothesized that ROS overproduction was secondary to the impaired responses to hypoxia due to the inhibi...
Alternative Titles
Full title
Repression of hypoxia-inducible factor-1 contributes to increased mitochondrial reactive oxygen species production in diabetes
Authors, Artists and Contributors
Author / Creator
Narayanan, Sampath
Xu, Cheng
Eliasson Angelstig, Sofie
Grünler, Jacob
Zhao, Allan
Di Toro, Alessandro
Bernardi, Luciano
Mazzone, Massimiliano
Carmeliet, Peter
Del Sole, Marianna
Solaini, Giancarlo
Forsberg, Elisabete A
Zhang, Ao
Brismar, Kerstin
Schiffer, Tomas A
Rajamand Ekberg, Neda
Botusan, Ileana Ruxandra
Palm, Fredrik
Catrina, Sergiu-Bogdan
Identifiers
Primary Identifiers
Record Identifier
TN_cdi_doaj_primary_oai_doaj_org_article_de99ad9d49774afc98f983792fb23b0a
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_de99ad9d49774afc98f983792fb23b0a
Other Identifiers
ISSN
2050-084X
E-ISSN
2050-084X
DOI
10.7554/eLife.70714
