Cardiac mitochondrial dysfunction during hyperglycemia - the role of oxidative stress and p66Shc signaling.
PBN-AR
Instytucja
Instytut "Pomnik - Centrum Zdrowia Dziecka"
Informacje podstawowe
Główny język publikacji
en
Czasopismo
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
ISSN
1357-2725
EISSN
1878-5875
Wydawca
Elsevier
Rok publikacji
2013
Numer zeszytu
1
Strony od-do
114-122
Numer tomu
45
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Autorzy
Pozostali autorzy
+ 9
Słowa kluczowe
en
hyperglycemia;
mitochondrial dysfunction;
ROS;
p66Shc
Streszczenia
Język
en
Treść
Diabetes mellitus is a chronic disease caused by a deficiency in the production of insulin and/or by the effects of insulin resistance. Insulin deficiency leads to hyperglycemia which is the major initiator of diabetic cardiovascular complications escalating with time and driven by many complex biochemical and molecular processes. Four hypotheses, which propose mechanisms of diabetes-associated pathophysiology, are currently considered. Cardiovascular impairment may be caused by an increase in polyol pathway flux, by intracellular advanced glycation end-products formation or increased flux through the hexosamine pathway. The latter of these mechanisms involves activation of the protein kinase C. Cellular and mitochondrial metabolism alterations observed in the course of diabetes are partially associated with an excessive production of reactive oxygen species (ROS). Among many processes and factors involved in ROS production, the 66 kDa isoform of the growth factor adaptor shc (p66Shc protein) is of particular interest. This protein plays a key role in the control of mitochondria-dependent oxidative balance thus it involvement in diabetic complications and other oxidative stress based pathologies is recently intensively studied. In this review we summarize the current understanding of hyperglycemia induced cardiac mitochondrial dysfunction with an emphasis on the oxidative stress and p66Shc protein. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy.
Cechy publikacji
Artykuł przeglądowy
Inne
System-identifier
0000012262
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