Chapter Hyperglycemia-Induced Endothelial Dysfunction (Record no. 38113)

MARC details
000 -LEADER
fixed length control field 02861naaaa2200265uu 4500
001 - CONTROL NUMBER
control field https://directory.doabooks.org/handle/20.500.12854/70272
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number intechopen.71433
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.5772/intechopen.71433
Terms of availability doi
041 0# - LANGUAGE CODE
Language code of text/sound track or separate title English
042 ## - AUTHENTICATION CODE
Authentication code dc
072 #7 - SUBJECT CATEGORY CODE
Subject category code MJD
Source bicssc
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Gero, Domokos
Relationship auth
245 10 - TITLE STATEMENT
Title Chapter Hyperglycemia-Induced Endothelial Dysfunction
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Name of publisher, distributor, etc. InTechOpen
Date of publication, distribution, etc. 2018
506 0# - RESTRICTIONS ON ACCESS NOTE
Terms governing access Open Access
Source of term star
Standardized terminology for access restriction Unrestricted online access
520 ## - SUMMARY, ETC.
Summary, etc. Glucose-induced endothelial dysfunction plays a fundamental role in the development of diabetic vascular complications and glycemic control (the foundation of diabetes care) provides limited protection against the cardiovascular complications. Therefore, identification of novel drug targets and treatment approaches for diabetes complications represent a key direction of current pharmaceutical research. The “unifying theory” of hyperglycemia-induced endothelial cell injury organizes the events of cellular dysfunction in a linear cascade and identifies mitochondrial superoxide generation as the triggering event of the injury. Exposure to high glucose concentration for long periods or repeated glycemic swings may induce changes in metabolic substrate availability and lead to mitochondrial hyperpolarization. Changes in the mitochondrial membrane potential induce superoxide production by the electron transport chain and result in oxidative stress. Mitochondrial superoxide is also responsible for the induction of other sources of reactive oxygen species (ROS) within the cells, including advanced glycation end products (AGEs) and the NADPH oxidase. Mitochondria also show morphological changes and impaired assembly of the respiratory complexes occurs, which results in cellular energy failure, cell senescence and vascular dysfunction. Current intervention strategies aim to inhibit the mitochondrial ROS production and novel therapeutic approaches are expected to provide valuable tools in diabetes therapy in the upcoming years.
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE
Terms governing use and reproduction Creative Commons
Use and reproduction rights https://creativecommons.org/licenses/by/3.0/
Source of term cc
-- https://creativecommons.org/licenses/by/3.0/
546 ## - LANGUAGE NOTE
Language note English
650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element Cardiovascular medicine
Source of heading or term bicssc
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term hyperglycemia, diabetes, endothelial cells, oxidative stress, mitochondria, electron transport chain, superoxide, bioenergetics
773 10 - HOST ITEM ENTRY
Host Biblionumber OAPEN Library ID: ONIX_20210602_10.5772/intechopen.71433_371
Control subfield nnaa
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://library.oapen.org/bitstream/20.500.12657/49257/1/57915.pdf">https://library.oapen.org/bitstream/20.500.12657/49257/1/57915.pdf</a>
Access status 0
Public note DOAB: download the publication
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://library.oapen.org/bitstream/20.500.12657/49257/1/57915.pdf">https://library.oapen.org/bitstream/20.500.12657/49257/1/57915.pdf</a>
Access status 0
Public note DOAB: download the publication
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://directory.doabooks.org/handle/20.500.12854/70272">https://directory.doabooks.org/handle/20.500.12854/70272</a>
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Public note DOAB: description of the publication

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