Endothelial cells cope with hypoxia-induced depletion of ATP via activation of cellular purine turnover and phosphotransfer networks.

A1 Journal article (refereed)

Internal Authors/Editors

Publication Details

List of Authors: Losenkova, Zuccarini, Helenius, Jacquemet, Gerasimovskaya, Tallgren, Jalkanen, Yegutkin
Publication year: 2018
Journal: BBA - Molecular Basis of Disease
Journal acronym: Biochim Biophys Acta Mol Basis Dis
Volume number: 1864
Issue number: 5 Pt A
Start page: 1804
End page: 1815
ISSN: 0925-4439


H]ADP/ATP. Furthermore, following a period of hypoxia, HUVEC underwent concurrent changes in intracellular signaling manifested in the depletion of putative ATP stores and targeted up-regulation of phospho-p53, p70S6K/mTOR and other tyrosine kinases. The revealed complex implication of both extrinsic and intrinsic mechanisms into a tuned hypoxia-induced control of purine homeostasis and signaling may open up further research for the development of pharmacological treatments to improve endothelial cell function under disease conditions associated with a loss of cellular ATP during oxygen deprivation.

Last updated on 2020-02-06 at 04:18