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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
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