Emerging Role of LncRNA Regulation for NLRP3 Inflammasome in Diabetes Complications

Abstract

Diabetes is a widespread metabolic disease with various complications, including diabetic nephropathy, retinopathy, cardiomyopathy, and other cardiovascular or cerebrovascular diseases. As the prevalence of diabetes increases in all age groups worldwide, diabetes and its complications cause an emerging public health burden. NLRP3 inflammasome is a complex of several proteins that play a critical role in inflammatory response and various diseases, including diabetes and its complications. Accumulating evidences indicate that NLRP3 inflammasome contributes to the development of diabetes and diabetic complications and that NLRP3 inflammation inactivation is beneficial in treating these illnesses. Emerging evidences suggest the critical role of long non-coding RNAs (lncRNAs) in regulating NLRP3 inflammasome activity in various diseases. LncRNAs are non-coding RNAs exceeding 200 nucleotides in length. Its dysregulation has been linked to the development of diseases, including diabetes. Recently, growing evidences hint that regulating lncRNAs on NLRP3 inflammasome is critical in developing and progressing diabetes and diabetic complications. Here, we discuss the role of lncRNAs in regulating NLRP3 inflammasome as well as its participation in diabetes and diabetic complications, providing novel insights into developing future therapeutic approaches for diabetes.

Long non-coding RNA L13Rik promotes high glucose-induced mesangial cell injury by regulating miR-2861/CDKN1B axis

“…In an addition, the effect of L13Rik on DN progression will be investigated in diabetic rats. Mounting studies have demonstrated that lncRNA functions as important mediator in DN or other diabetic complications (Lu et al, 2021). For instance, lncRNA MSC-AS1 is up-regulated in peripheral blood from DN patients, and MSC-AS1 silencing alleviates HG-triggered MC proliferation, fibrosis, and inflammation through sponging miR-325 and de-repressing cyclin G1 (Zhao et al, 2022).…”

Diabetes Mellitus Promotes the Development of Atherosclerosis: The Role of NLRP3

“…The overexpression of pro-inflammatory factors may further induce DM complications (31). In recent years, multiple studies have suggested that NLRP3 inflammasome is related to DM and its complications (32). For example, Tseng et al demonstrated that hyperglycemia high glucose induces activation of NLRP3-ASC inflammasome, leading to casparase-1 activation and secretion of IL-1b and IL-18 in human monocyte cell lines (33).…”

“…The overexpression of pro-inflammatory factors may further induce DM complications ( 31 ). In recent years, multiple studies have suggested that NLRP3 inflammasome is related to DM and its complications ( 32 ). For example, Tseng et al.…”

Advances in the therapeutic application and pharmacological properties of kinsenoside against inflammation and oxidative stress-induced disorders

“…Specifically, inflammatory factors decrease the activities of insulin receptor in hepatocytes, muscle cells, and adipocytes, accompanied by insulin receptor substance-induced intracellular signaling transduction inhibition, glucose transporter generation and translocation suppression, and glucose uptake and metabolism disruption ( Passarelli and Machado, 2021 ; Xiao et al, 2022 ). A hyperglycemic environment facilitates the occurrence of inflammation and oxidative stress, which exacerbate vascular and myocardial complications and enhance the risks of diabetic disability and mortality ( Lu et al, 2021 ; Semwal et al, 2021 ; Yu et al, 2022 ). There is evidence showing that KD administration effectively decreased blood glucose content, elevated circulating insulin level, prevented weight gain, and improved glucose tolerance in streptozotocin-induced hyperglycemic rats, without causing toxicity.…”