Abstract

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.

摘要

脂肪组织中脂质的过度积累通过影响细胞过程来破坏代谢稳态。内质网 (ER) 应激是受肥胖影响的此类过程之一。肥胖引起的脂肪组织的生化和生理变化会干扰脂肪 ER 功能，从而导致 ER 应激。这与炎症和自噬等其他细胞过程的不规则性增加一致，从而影响脂肪细胞内的整体代谢完整性。此外，可以在转录后调节基因的 microRNA (miRNA) 在肥胖症中受到不同程度的调节。更好地理解和识别此类 miRNA 可用作抗击疾病的新治疗靶点。在本次审查中，我们讨论了 ER 应激作为常见分子过程参与肥胖相关代谢紊乱发病机制的方式。此外，我们的综述讨论了详细的潜在机制，通过这些机制，ER 应激和 miRNA 有助于肥胖患者脂肪组织的代谢改变。因此，确定 miRNAs-ER 应激串扰在肥胖期间调节脂肪功能的机制可用作对抗包括肥胖在内的慢性疾病的潜在治疗方法。