Mitochondrial mechanisms of endothelial dysfunction
PBN-AR
Instytucja
Wydział Biologii (Uniwersytet im. Adama Mickiewicza w Poznaniu)
Źródłowe zdarzenia ewaluacyjne
Informacje podstawowe
Główny język publikacji
en
Czasopismo
Pharmacological Reports
ISSN
1734-1140
EISSN
Wydawca
Elsevier Sp. z o.o.
DOI
Rok publikacji
2015
Numer zeszytu
Strony od-do
704-710
Numer tomu
67
Identyfikator DOI
Liczba arkuszy
Słowa kluczowe
en
Endothelial dysfunction
Mitochondria
Reactive oxygen species
Mitochondrial potassium channels
Uncoupling protein
Streszczenia
Język
en
Treść
Endothelial cells play an important physiological role in vascular homeostasis. They are also the first barrier that separates blood from deeper layers of blood vessels and extravascular tissues. Thus, they are exposed to various physiological blood components as well as challenged by pathological stimuli, which may exert harmful effects on the vascular system by stimulation of excessive generation of reactive oxygen species (ROS). The major sources of ROS are NADPH oxidase and mitochondrial respiratory chain complexes. Modulation of mitochondrial energy metabolism in endothelial cells is thought to be a promising target for therapy in various cardiovascular diseases. Uncoupling protein 2 (UCP2) is a regulator of mitochondrial ROS generation and can antagonise oxidative stress-induced endothelial dysfunction. Several studies have revealed the important role of UCP2 in hyperglycaemia-induced modifications of mitochondrial function in endothelial cells. Additionally, potassium fluxes through the inner mitochondrial membrane, which are involved in ROS synthesis, affect the mitochondrial volume and change both the mitochondrial membrane potential and the transport of calcium into the mitochondria. In this review, we concentrate on the mitochondrial role in the cytoprotection phenomena of endothelial cells.
Cechy publikacji
ORIGINAL_ARTICLE
Inne
System-identifier
614592
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