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Kovacs et al. Vessel Plus 2018;2:15                                         Vessel Plus
               DOI: 10.20517/2574-1209.2018.06




               Review                                                                        Open Access


               Histone deacetylases in vascular permeability and
               remodeling associated with acute lung injury


               Laszlo Kovacs , Anita Kovacs-Kasa , Alexander D. Verin , David Fulton , Rudolf Lucas 1,2,3 , Yunchao
                                               2,#
                            1,#
                                                                 2,3
                                                                              1,2
               Su 1,2,3,4
               1 Department of Pharmacology & Toxicology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
               2 Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
               3 Department of Medicine, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
               4 Research Service, Charlie Norwood Veterans Affairs Medical Center, Augusta, GA 30912, USA.
               # Authors contributed equally.
               Correspondence to: Dr. Yunchao Su, Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta
               University, 1120 15th Street, Augusta, GA 30912, USA. E-mail: ysu@augusta.edu
               How to cite this article: Kovacs L, Kovacs-Kasa A, Verin AD, Fulton D, Lucas R, Su Y. Histone deacetylases in vascular permeability
               and remodeling associated with acute lung injury. Vessel Plus 2018;2:15. http://dx.doi.org/10.20517/2574-1209.2018.06

               Received: 1 Mar 2018    First Decision: 20 Jun 2018    Revised: 28 Jun 2018    Accepted: 30 Jun 2018    Published: 10 Jul 2018

               Science Editor: Evgenia V. Gerasimovskaya    Copy Editor: Jun-Yao Li    Production Editor: Huan-Liang Wu


               Abstract
               Acute lung injury (ALI) is a severe progressive disorder that arises from a wide range of causes such as toxins or
               inflammation, resulting in significant morbidity and mortality. There are no effective therapeutic options apart from
               mechanical ventilation strategies. While the mechanisms that govern the clinically relevant process of increased
               endothelial cell (EC) permeability and remodeling associated with ALI are under intense investigation, our knowledge
               of the processes that determine barrier enhancement or preservation are far from completion. Recently, epigenetic
               mechanisms have emerged as a major regulator of enduring changes in cell behavior and the therapeutic potential of
               inhibiting histone deacetylases (HDACs) for the treatment of cardiovascular and inflammatory diseases has gained
               remarkable attention. Although HDACs have been shown to play an important role in regulating EC barrier function, the
               involved HDAC subtypes and mechanisms remain undefined. Further investigation of the HDAC signaling may provide
               therapeutic approaches for the prevention and treatment of ALI.

               Keywords: Acute lung injury, endothelial barrier function, histone deacetylases



               INTRODUCTION
               Acute lung injury (ALI) is a significant source of morbidity and mortality with over 200,000 incidences
                               [1,2]
               per year in the US . ALI arises from a wide range of causes such as toxins or inflammation resulting in

                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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