Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

被引：29

作者：

Chen, Xiaona ^{[1
,2
]}

He, Yanhong ^{[2
]}

Fu, Wenjun ^{[2
]}

Sahebkar, Amirhossein ^{[3
,4
,5
]}

Tan, Yuhui ^{[1
,2
]}

Xu, Suowen ^{[6
]}

Li, Hong ^{[1
,2
]}

机构：

[1] Guangzhou Univ Chinese Med, Sch Basic Med Sci, Dept Med Biotechnol, Guangzhou, Peoples R China

[2] Guangzhou Univ Chinese Med, Res Ctr Basic Integrat Med, Guangzhou, Peoples R China

[3] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Razavi Khorasan, Iran

[4] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Razavi Khorasan, Iran

[5] Polish Mothers Mem Hosp Res Inst, Lodz, Poland

[6] Univ Sci & Technol China, Div Life Sci & Med, Dept Endocrinol, Affiliated Hosp 1, Hefei, Peoples R China

来源：

FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY | 2020年 / 8卷

基金：

中国国家自然科学基金;

关键词：

atherosclerosis; endothelial dysfunction; smooth muscle cells; macrophage; epigenetic; histone deacetylation; HDAC inhibitors; SMOOTH-MUSCLE-CELLS; NITRIC-OXIDE SYNTHASE; CHAIN FATTY-ACIDS; ACUTE LUNG INJURY; ENDOTHELIAL-CELLS; GENE-EXPRESSION; ANGIOTENSIN-II; OXIDATIVE STRESS; VASCULAR ENDOTHELIUM; PLATELET ACTIVATION;

D O I：

10.3389/fcell.2020.581015

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Atherosclerosis (AS), the most common underlying pathology for coronary artery disease, is a chronic inflammatory, proliferative disease in large- and medium-sized arteries. The vascular endothelium is important for maintaining vascular health. Endothelial dysfunction is a critical early event leading to AS, which is a major risk factor for stroke and myocardial infarction. Accumulating evidence has suggested the critical roles of histone deacetylases (HDACs) in regulating vascular cell homeostasis and AS. The purpose of this review is to present an updated view on the roles of HDACs (Class I, Class II, Class IV) and HDAC inhibitors in vascular dysfunction and AS. We also elaborate on the novel therapeutic targets and agents in atherosclerotic cardiovascular diseases.

引用

页数：17

共 226 条

[1] Salt-inducible kinase induces cytoplasmic histone deacetylase 4 to promote vascular calcification [J].

Abend, Alon ;

Shkedi, Omer ;

Fertouk, Michal ;

Caspi, Lilac H. ;

Kehat, Izhak .

EMBO REPORTS, 2017, 18 (07) :1166-1185

[2] Inhibition of HDAC6 Attenuates Diabetes-Induced Retinal Redox Imbalance and Microangiopathy [J].

Abouhish, Hossameldin ;

Thounaojam, Menaka C. ;

Jadeja, Ravirajsinh N. ;

Gutsaeva, Diana R. ;

Powell, Folami L. ;

Khriza, Mohamed ;

Martin, Pamela M. ;

Bartoli, Manuela .

ANTIOXIDANTS, 2020, 9 (07) :1-19

[3] Galectin-9 Protein Expression in Endothelial Cells Is Positively Regulated by Histone Deacetylase 3 [J].

Alam, Saydul ;

Li, Hongling ;

Margariti, Andriana ;

Martin, Daniel ;

Zampetaki, Anna ;

Habi, Ouassila ;

Cockerill, Gillian ;

Hu, Yanhua ;

Xu, Qingbo ;

Zeng, Lingfang .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (51) :44211-44217

[4] Metabolism: The road to inflammation and atherosclerosis [J].

Ali, Lubna ;

Schnitzler, Johan G. ;

Kroon, Jeffrey .

CURRENT OPINION IN LIPIDOLOGY, 2018, 29 (06) :475-481

[5] Role of matrix metalloproteinases and histone deacetylase in oxidative stress-induced degradation of the endothelial glycocalyx [J].

Ali, Mohamed M. ;

Mahmoud, Abeer M. ;

Le Master, Elizabeth ;

Levitan, Irena ;

Phillips, Shane A. .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2019, 316 (03) :H647-H663

[6] NONINVASIVE DETECTION OF EARLY ENDOTHELIAL DYSFUNCTION IN HYPERCHOLESTEROLEMIC SUBJECTS [J].

ARCARO, G ;

ZENERE, BM ;

TRAVIA, D ;

ZENTI, MG ;

COVI, G ;

LECHI, A ;

MUGGEO, M .

ATHEROSCLEROSIS, 1995, 114 (02) :247-254

[7] Histone Deacetylase 9 Activates IKK to Regulate Atherosclerotic Plaque Vulnerability [J].

Asare, Yaw ;

Campbell-James, Thomas A. ;

Bokov, Yury ;

Yu, Lydia Luya ;

Prestel, Matthias ;

El Bounkari, Omar ;

Roth, Stefan ;

Megens, Remco T. A. ;

Straub, Tobias ;

Thomas, Kyra ;

Yan, Guangyao ;

Schneider, Melanie ;

Ziesch, Natalie ;

Tiedt, Steffen ;

Silvestre-Roig, Carlos ;

Braster, Quinte ;

Huang, Yishu ;

Schneider, Manuela ;

Malik, Rainer ;

Haffner, Christof ;

Liesz, Arthur ;

Soehnlein, Oliver ;

Bernhagen, Juergen ;

Dichgans, Martin .

CIRCULATION RESEARCH, 2020, 127 (06) :811-823

[8] Trichostatin A, an HDAC Class I/II, Inhibitor, Promotes Pi-Induced Vascular Calcification Via Up-Regulation of the Expression of Alkaline Phosphatase [J].

Azechi, Takuya ;

Kanehira, Dan ;

Kobayashi, Takashi ;

Sudo, Ryo ;

Nishimura, Akiko ;

Sato, Fumiaki ;

Wachi, Hiroshi .

JOURNAL OF ATHEROSCLEROSIS AND THROMBOSIS, 2013, 20 (06) :538-547

[9] Deficiency of the Stroke Relevant HDAC9 Gene Attenuates Atherosclerosis in Accord With Allele-Specific Effects at 7p21.1 [J].

Azghandi, Sepiede ;

Prell, Caroline ;

van der Laan, Sander W. ;

Schneider, Manuela ;

Malik, Rainer ;

Berer, Kerstin ;

Gerdes, Norbert ;

Pasterkamp, Gerard ;

Weber, Christian ;

Haffner, Christof ;

Dichgans, Martin .

STROKE, 2015, 46 (01) :197-+

[10] Macrophages Generate Reactive Oxygen Species in Response to Minimally Oxidized Low-Density Lipoprotein Toll-Like Receptor 4-and Spleen Tyrosine Kinase-Dependent Activation of NADPH Oxidase 2 [J].

Bae, Yun Soo ;

Lee, Jee Hyun ;

Choi, Soo Ho ;

Kim, Sunah ;

Almazan, Felicidad ;

Witztum, Joseph L. ;

Miller, Yury I. .

CIRCULATION RESEARCH, 2009, 104 (02) :210-U147

← 1 2 3 4 5 6 7 8 9 10 →