Duisenbek Ayauly, Lopez-Armas Gabriela C, Pérez Miguel, Avilés Pérez María D, Aguilar Benitez José Miguel, Pereira Pérez Víctor Roger, Gorts Ortega Juan, Yessenbekova Arailym, Ablaikhanova Nurzhanyat, Escames Germaine, Acuña-Castroviejo Darío, Rusanova Iryna
Department of Biophysics, Biomedicine and Neuroscience, Al-Farabi Kazakh National University, Al-Farabi Av. 71, Almaty 050040, Kazakhstan.
Department of Biochemistry and Molecular Biology I, Faculty of Science, University of Granada, 18019 Granada, Spain.
Antioxidants (Basel). 2023 Jun 16;12(6):1290. doi: 10.3390/antiox12061290.
A common denominator of metabolic diseases, including type 2 diabetes Mellitus, dyslipidemia, and atherosclerosis, are elevated oxidative stress and chronic inflammation. These complex, multi-factorial diseases are caused by the detrimental interaction between the individual genetic background and multiple environmental stimuli. The cells, including the endothelial ones, acquire a preactivated phenotype and metabolic memory, exhibiting increased oxidative stress, inflammatory gene expression, endothelial vascular activation, and prothrombotic events, leading to vascular complications. There are different pathways involved in the pathogenesis of metabolic diseases, and increased knowledge suggests a role of the activation of the NF-kB pathway and NLRP3 inflammasome as key mediators of metabolic inflammation. Epigenetic-wide associated studies provide new insight into the role of microRNAs in the phenomenon of metabolic memory and the development consequences of vessel damage. In this review, we will focus on the microRNAs related to the control of anti-oxidative enzymes, as well as microRNAs related to the control of mitochondrial functions and inflammation. The objective is the search for new therapeutic targets to improve the functioning of mitochondria and reduce oxidative stress and inflammation, despite the acquired metabolic memory.
包括2型糖尿病、血脂异常和动脉粥样硬化在内的代谢性疾病的一个共同特征是氧化应激升高和慢性炎症。这些复杂的多因素疾病是由个体遗传背景与多种环境刺激之间的有害相互作用引起的。包括内皮细胞在内的细胞获得一种预激活表型和代谢记忆，表现出氧化应激增加、炎症基因表达、内皮血管激活和血栓形成前事件，从而导致血管并发症。代谢性疾病的发病机制涉及不同的途径，越来越多的知识表明NF-κB途径和NLRP3炎性小体的激活作为代谢炎症的关键介质发挥作用。全表观基因组关联研究为微小RNA在代谢记忆现象和血管损伤的发展后果中的作用提供了新的见解。在本综述中，我们将重点关注与抗氧化酶控制相关的微小RNA，以及与线粒体功能和炎症控制相关的微小RNA。目标是寻找新的治疗靶点，以改善线粒体功能，减少氧化应激和炎症，尽管存在获得性代谢记忆。
