Laboratory of Nutrigenomics, Inflammation and Obesity Research, Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.
Obesity Research Institute, Texas Tech University, Lubbock, TX, USA.
Crit Rev Biochem Mol Biol. 2021 Oct;56(5):455-481. doi: 10.1080/10409238.2021.1925219. Epub 2021 Jun 28.
Over accumulation of lipids in adipose tissue disrupts metabolic homeostasis by affecting cellular processes. Endoplasmic reticulum (ER) stress is one such process affected by obesity. Biochemical and physiological alterations in adipose tissue due to obesity interfere with adipose ER functions causing ER stress. This is in line with increased irregularities in other cellular processes such as inflammation and autophagy, affecting overall metabolic integrity within adipocytes. Additionally, microRNAs (miRNAs), which can post-transcriptionally regulate genes, are differentially modulated in obesity. A better understanding and identification of such miRNAs could be used as novel therapeutic targets to fight against diseases. In this review, we discuss ways in which ER stress participates as a common molecular process in the pathogenesis of obesity-associated metabolic disorders. Moreover, our review discusses detailed underlying mechanisms through which ER stress and miRNAs contribute to metabolic alteration in adipose tissue in obesity. Hence, identifying mechanistic involvement of miRNAs-ER stress cross-talk in regulating adipose function during obesity could be used as a potential therapeutic approach to combat chronic diseases, including obesity.
脂肪组织中脂质的过度积累通过影响细胞过程破坏代谢稳态。内质网（ER）应激就是受肥胖影响的这样一个过程。肥胖导致脂肪组织的生化和生理改变干扰脂肪 ER 功能，引起 ER 应激。这与其他细胞过程（如炎症和自噬）的不规则性增加是一致的，影响了脂肪细胞内的整体代谢完整性。此外，microRNAs（miRNAs）可以通过转录后调节基因，在肥胖中被差异化调节。更好地理解和鉴定这些 miRNAs 可以作为治疗疾病的新靶点。在这篇综述中，我们讨论了 ER 应激作为肥胖相关代谢紊乱发病机制中的共同分子过程的参与方式。此外，我们的综述还讨论了 ER 应激和 miRNAs 如何通过详细的潜在机制导致肥胖中脂肪组织代谢改变。因此，确定 miRNA-ER 应激相互作用在肥胖期间调节脂肪功能的机制参与可能被用作对抗包括肥胖在内的慢性疾病的潜在治疗方法。
