Therapeutic potential of ALKB homologs for cardiovascular disease

被引:18
作者
Xiao, Ming-Zhu [1 ,2 ]
Liu, Jia-Ming [1 ,2 ]
Xian, Cui-Ling [1 ,3 ]
Chen, Keng-Yu [1 ,4 ]
Liu, Zhong-Qiu [1 ]
Cheng, Yuan-Yuan [1 ]
机构
[1] Guangzhou Univ Chinese Med, Guangdong Key Lab Translat Canc Res Chinese Med, Joint Lab Translat Canc Res Chinese Med,Sch Pharm, Minist Educ Peoples Republ China,Int Inst Transla, Guangzhou 510006, Guangdong, Peoples R China
[2] Guangdong Pharmaceut Univ, Sch Pharm, Guangzhou 510006, Peoples R China
[3] Guangdong Pharmaceut Univ, Sch Tradit Chinese Med, Guangzhou 510006, Peoples R China
[4] Guangdong Pharmaceut Univ, Affiliated Hosp 2, Yunfu 527300, Peoples R China
基金
中国国家自然科学基金;
关键词
Cardiovascular diseases; ALKB homologs; RNA demethylation; DNA demethylation; Oxidative stress; Therapy; DNA-REPAIR ENZYMES; DEMETHYLASE ALKBH5; MOLECULAR-MECHANISMS; CRYSTAL-STRUCTURE; HEART-DISEASE; CELL-DEATH; RNA; PROTEIN; MACROPHAGES; RECOGNITION;
D O I
10.1016/j.biopha.2020.110645
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Cardiovascular diseases (CVDs) are the leading causes of human death. Recently, ALKB homologs, including ALKBH1-8 and FTO, have been found to have a variety of biological functions, such as histone demethylation, RNA demethylation, and DNA demethylation. These functions may regulate the physiological and pathological processes of CVDs, including inflammation, oxidative stress, cell apoptosis, and mitochondrial, endothelial, and fat metabolism dysfunction. In the present review, we summarize the biological functions of ALKB homologs and the relationship between the ALKB homologs and CVDs. Importantly, we discuss the roles of ALKB homologs in the regulation of oxidative stress, inflammation, autophagy, and DNA damage in CVDs, as well as the practical applications of ALKB homologs inhibitors or agonists in treating CVDs. In conclusion, the ALKBH family might be a promising target for CVDs therapy.
引用
收藏
页数:11
相关论文
共 137 条
[41]   FTO Genotype, Physical Activity, and Coronary Heart Disease Risk in Swedish Men and Women [J].
Gustavsson, Jaana ;
Mehlig, Kirsten ;
Leander, Karin ;
Lissner, Lauren ;
Bjorck, Lena ;
Rosengren, Annika ;
Nyberg, Fredrik .
CIRCULATION-CARDIOVASCULAR GENETICS, 2014, 7 (02) :171-177
[42]   NSUN3 and ABH1 modify the wobble position of mt-tRNAMet to expand codon recognition in mitochondrial translation [J].
Haag, Sara ;
Sloan, Katherine E. ;
Ranjan, Namit ;
Warda, Ahmed S. ;
Kretschmer, Jens ;
Blessing, Charlotte ;
Huebner, Benedikt ;
Seikowski, Jan ;
Dennerlein, Sven ;
Rehling, Peter ;
Rodnina, Marina V. ;
Hoebartner, Claudia ;
Bohnsack, Markus T. .
EMBO JOURNAL, 2016, 35 (19) :2104-2119
[43]   Crystal structure of the FTO protein reveals basis for its substrate specificity [J].
Han, Zhifu ;
Niu, Tianhui ;
Chang, Junbiao ;
Lei, Xiaoguang ;
Zhao, Mingyan ;
Wang, Qiang ;
Cheng, Wei ;
Wang, Jinjing ;
Feng, Yi ;
Chai, Jijie .
NATURE, 2010, 464 (7292) :1205-U129
[44]   Functions of N6-methyladenosine and its role in cancer [J].
He, Liuer ;
Li, Huiyu ;
Wu, Anqi ;
Peng, Yulong ;
Shu, Guang ;
Yin, Gang .
MOLECULAR CANCER, 2019, 18 (01)
[45]  
He Y, 2018, GYNECOL ENDOCRINOL, V15, P1, DOI DOI 10.1186/s12974-017-1027-y
[46]   GR-mediated FTO transactivation induces lipid accumulation in hepatocytes via demethylation of m6A on lipogenic mRNAs [J].
Hu, Yun ;
Feng, Yue ;
Zhang, Luchu ;
Jia, Yimin ;
Cai, Demin ;
Qian, Shu-Bing ;
Du, Min ;
Zhao, Ruqian .
RNA BIOLOGY, 2020, 17 (07) :930-942
[47]   FTO Knockout Causes Chromosome Instability and G2/M Arrest in Mouse GC-1 Cells [J].
Huang, Tao ;
Gao, Qiang ;
Feng, Tongying ;
Zheng, Yi ;
Guo, Jiayin ;
Zeng, Wenxian .
FRONTIERS IN GENETICS, 2019, 9
[48]  
Ibáñez B, 2015, J AM COLL CARDIOL, V65, P1455, DOI 10.1016/j.jacc.2015.02.032
[49]   A critical review on diet-induced microbiota changes and cardiovascular diseases [J].
Jayachandran, Muthukumaran ;
Chung, Stephen Sum Man ;
Xu, Baojun .
CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION, 2020, 60 (17) :2914-2925
[50]   m6A demethylase ALKBH5 inhibits tumor growth and metastasis by reducing YTHDFs-mediated YAP expression and inhibiting miR-107/LATS2-mediated YAP activity in NSCLC [J].
Jin, Dan ;
Guo, Jiwei ;
Wu, Yan ;
Yang, Lijuan ;
Wang, Xiaohong ;
Du, Jing ;
Dai, Juanjuan ;
Chen, Weiwei ;
Gong, Kaikai ;
Miao, Shuang ;
Li, Xuelin ;
Sun, Hongliang .
MOLECULAR CANCER, 2020, 19 (01)