REV-ERBα MITIGATES HEART FAILURE BY EXERTING TRANSCRIPTIONAL REPRESSION: A LITERATURE REVIEW Heart failure (HF) is a major cause of mortality, affecting millions of people in the United States. Current treatments focus on minimizing stress and improving hemodynamics, but there is still a need for an effective strategy that can selectively inhibit the abnormal gene program associated with HF. Rev-erb, a member of the nuclear receptor superfamily, has been identified as a potential therapeutic target for HF due to its role in regulating circadian rhythm, glucose and lipid metabolism, and inflammation. Synthetic Rev-erb agonists have shown promise in preclinical studies, improving metabolic and inflammatory pathways while also enhancing mitochondrial function. Long-term therapy with these agonists has also been shown to reduce atherosclerotic plaque. While more research is needed to fully understand Rev-erb’s functions in HF development, it represents a potentially exciting new avenue for treatment. This literature review explores the potential use of Rev-erb agonists as a therapeutic target for HF patients.

Background: Heart failure (HF) is a complex clinical syndrome with signs and symptoms resulting from any structural dysfunction of ventricular filling or blood ejection. miRNAs were known as essential regulators and tissue-specifically expressed. MicroRNA-155 (miR-155) expression in macrophages is already well known to promote hypertrophy, cardiac inflammation, and failure due to pressure overload. In this study, we aim to identify the role of expression miR-155 as a potential biomarker for HF. Method: We incorporated search engines from Google Scholar, PubMed, EBSCO Host, and ProQuest to search the articles. Newcastle Ottawa Scale (NOS) was used to evaluate the bias risk in the case-control research. A systematic database search reveals 6 relevant studies. Results: This research found that miR-155 levels were significantly higher in heart failure patients than in the MI and control groups. MiR-155's plasma levels in heart failure are higher than the control group, with a cut-off value of 0.8591, a sensitivity value of 98.5%, and a specificity value of 64.6%. However, miRNA expression patterns do not appear to differ significantly between pf and cf LVAD. Most cardiac changes and clinical outcomes specific to each device are independent of differences in miRNA expression levels. According to one study, miR-155, a diagnostic biomarker for heart failure, had a specificity of 92.14% and a cutoff value of 1.77%. Conclusion Our systematic review showed that miR-155 could be a potential new diagnostic biomarker in HF patients.
MicroRNAs