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Journal of Cardiovascular Translational Research

Published in:

01-11-2014

The Role of Intrinsic Apoptotic Signaling in Hemorrhagic Shock-Induced Microvascular Endothelial Cell Barrier Dysfunction

Authors: Devendra A. Sawant, Binu Tharakan, Felicia A. Hunter, Ed W. Childs

Published in: Journal of Cardiovascular Translational Research | Issue 8/2014

Abstract

Hemorrhagic shock leads to endothelial cell barrier dysfunction resulting in microvascular hyperpermeability. Hemorrhagic shock-induced microvascular hyperpermeability is associated with worse clinical outcomes in patients with traumatic injuries. The results from our laboratory have illustrated a possible pathophysiological mechanism showing involvement of mitochondria-mediated “intrinsic” apoptotic signaling in regulating hemorrhagic shock-induced microvascular hyperpermeability. Hemorrhagic shock results in overexpression of Bcl-2 family of pro-apoptotic protein, BAK, in the microvascular endothelial cells. The increase in BAK initiates “intrinsic” apoptotic signaling cascade with the release of mitochondrial cytochrome c in the cytoplasm and activation of downstream effector caspase-3, leading to loss of endothelial cell barrier integrity. Thus, this review article offers a brief overview of important findings from our past and present research work along with new leads for future research. The summary of our research work will provide information leading to different avenues in developing novel strategies against microvascular hyperpermeability following hemorrhagic shock.

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Title: The Role of Intrinsic Apoptotic Signaling in Hemorrhagic Shock-Induced Microvascular Endothelial Cell Barrier Dysfunction
Authors: Devendra A. Sawant
Binu Tharakan
Felicia A. Hunter
Ed W. Childs
Publication date: 01-11-2014
Publisher: Springer US
Published in: Journal of Cardiovascular Translational Research / Issue 8/2014
Print ISSN: 1937-5387
Electronic ISSN: 1937-5395
DOI: https://doi.org/10.1007/s12265-014-9589-x

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The Role of Intrinsic Apoptotic Signaling in Hemorrhagic Shock-Induced Microvascular Endothelial Cell Barrier Dysfunction

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