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Therapeutic potential of ALKB homologs for cardiovascular disease
Ming-Zhu Xiao1, Jia-Ming Liu1, Cui-Ling Xian2
1Guangdong Key Laboratory for Translational Cancer Research of Chinese Medicine, Joint Laboratory for Translational Cancer Research of Chinese Medicine of the Ministry of Education of the People's Republic of China, International Institute for Translational Chinese Medicine, School of Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China; School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Insights
ALKB homologs, enzymes involved in demethylation, show potential in treating cardiovascular diseases (CVDs). Their roles in regulating inflammation and oxidative stress offer new therapeutic targets for CVDs.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiology
Background:
- Cardiovascular diseases (CVDs) are a major global health concern, representing the leading cause of mortality.
- ALKB homologs (ALKBH1-8 and FTO) are enzymes with diverse demethylation functions (histone, RNA, DNA).
Purpose of the Study:
- To review the biological functions of ALKB homologs.
- To explore the relationship between ALKB homologs and CVDs.
- To discuss the therapeutic potential of targeting ALKB homologs for CVDs.
Main Methods:
- Literature review of ALKB homologs' functions.
- Analysis of ALKB homologs' roles in CVD pathogenesis.
- Evaluation of ALKB homologs' therapeutic applications.
Main Results:
- ALKB homologs regulate key CVD processes like inflammation, oxidative stress, apoptosis, and metabolic dysfunction.
- These enzymes are implicated in DNA damage and autophagy within the context of CVDs.
Conclusions:
- ALKB homologs play significant roles in CVD development and progression.
- Targeting ALKB homologs with inhibitors or agonists presents a promising therapeutic strategy for CVDs.
Abstract:
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.
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