key genetic factors in the metabolic syndrome predisposition which may be a therapeutic options by gene therapy
Moataz Dowaidar
Abstract
Metabolic syndrome affects 24–42 percent of individuals over the age of 50 in the United States. Dietary treatments tailored to the APOE genotype may help patients with MeS. Both mitotic and meiotic epigenetics are heritable. SREBP 1 and 2 genes overexpress in response to low cholesterol, statins, and insulin tolerance, resulting in decreased fatty acid oxidation, insulin signalling, and HDL-c levels. FTO is a key gene in the metabolic syndrome predisposition which may be a therapeutic option. MicroRNA repression of the VEGF 62 reference gene is prevented by the LncRNA MIAT/miR-150-5p complex. MEG3, a maternally expressed three-letter noncoding RNA, has been related to endothelial cell angiogenesis. Phosphorylation of p38 and JNK improved in the absence of (SRA) lncRNAs, resulting in decreased insulin signaling. Mipomersen is a 20-mer oligonucleotide that binds to the APOB mRNA's coding region. Volanersorsen has finished phase II and III clinical trials, making it the first APOC3 ASO to do so. ASO targeting APOB3 based on next-generation ligands is also in the early stages of research. Angptl3 is another successful genome editing target. Given the role of ANGPTL3 in TRL metabolism. Defects in the LDLR gene cause the most common genetic form of hypercholesterolemia, FH.