Jackson Ampadu-Okyere, Regine Mugwaneza Annick, Subrata Chakrabarti, Long Shiyin
Research lab of translational medicine, Medical school, University of South China, Hengyang, Hunan Province 421001, China.
International college, University of South China, Hengyang, Hunan Province 421001, China.
Int J Cardiol Heart Vasc. 2018 Sep 25;21:36-44. doi: 10.1016/j.ijcha.2018.09.006. eCollection 2018 Dec.
Atherosclerosis (AS) manifested by lipid accumulation, extracellular matrix protein deposition, and calcification in the intima and media of the large to medium size arteries promoting arterial stiffness and reduction of elasticity. It has been accepted that AS leads to increased morbidity and mortality worldwide. Recent studies indicated that genetic abnormalities play an important role in the development of AS. Specific genetic mutation and histone modification have been found to induce AS formation. Furthermore, specific RNAs such as microRNAs and circular RNAs have been identified to play a crucial role in the progression of AS. Nevertheless, the mechanisms by which genetic mutation, DNA and histone modification, microRNAs and circular RNA induce AS still remain elusive. This review describes specific mechanisms and pathways through which genetic mutation, DNA and histone modification, microRNAs and circular RNA instigate AS. This review further provides a therapeutic strategic direction for the treatment of AS targeting genetic mechanisms.
动脉粥样硬化（AS）表现为大中动脉内膜和中膜脂质蓄积、细胞外基质蛋白沉积及钙化，导致动脉僵硬和弹性降低。全世界都已公认AS会导致发病率和死亡率上升。近期研究表明，基因异常在AS的发生发展中起重要作用。已发现特定基因突变和组蛋白修饰可诱导AS形成。此外，已确定特定RNA，如微小RNA和环状RNA在AS进展中起关键作用。然而，基因突变、DNA和组蛋白修饰、微小RNA和环状RNA诱导AS的机制仍不清楚。本综述描述了基因突变、DNA和组蛋白修饰、微小RNA和环状RNA引发AS的具体机制和途径。本综述还针对以遗传机制为靶点的AS治疗提供了治疗策略方向。
