Acute myocardial infarction (AMI) is the leading cause of sudden death worldwide. MicroRNA-155 (miR-155) has been reported to target antiapoptotic genes in various diseases models, but the functional role of miR-155 in response to MI injury needs further investigations. This study investigated the role of miR-155 in myocardial ischemia injury. TUNEL and flow cytometry were performed to measure cell apoptosis. Western blot analysis was employed to detect protein expressions of Bcl-2, XIAP, Bax, and caspase-3. qRT-PCR was used to quantify miRNA levels. We showed that miR-155 was dynamically elevated in murine hearts subjected to MI and in neonatal rat ventricular cardiomyocyte (NRVM) injury induced by hydrogen peroxide (H₂O₂). In response to H₂O₂, the silencing of miR-155 using AMO-155 (antisense inhibitor oligodeoxyribonucleotides) significantly increased cell viability and reduced cell apoptosis. Moreover, AMO-155 reversed the H₂O₂-induced downregulation of Bcl-2 and XIAP and upregulation of Bax and cleaved-caspase-3. Further study revealed that AMO-155 resulted in a decrease of H₂O₂-induced JC-1-labelled monomeric cell number. In addition, AMO-155 markedly decreased infarct size, ameliorated impaired cardiac function, and significantly reduced apoptotic cell percentages in MI mice heart. The RNA-binding protein Quaking (QKI) was predicted as a target gene of miR-155 through bioinformatic analysis, and AMO-155 attenuated the downregulation of QKI in H₂O₂-treated cardiomyocytes and MI mice heart. Knockdown of QKI by siRNA abolished the antiapoptotic effects of AMO-155. Taken together, miR-155 is upregulated in the MI heart and NRVMs in response to H₂O₂stress, and downregulating of miR-155 protects cardiomyocytes against apoptosis. Mechanistically, it is probably due to the repression of QKI signaling pathway.

Clinical studies after marketing have shown that the use of glucagon-like peptide-1 receptor agonist(GLP-1RA) may lead to acute kidney injury(AKI). However, few epidemiological studies have investigated the risk, clinical features, and outcomes of AKI caused by different GLP-1RA. In this study, Adverse Event Reporting System (FAERS) data were used to compare the association between different GLP-1RA and AKI in the real world.Methods: FAERS data from January 2004 to December 2021 were mined using disproportionality analysis and Bayesian analysis to determine the correlation between different GLP-1RA and AKI, and the onset time, mortality, and hospitalization rate of different GLP-1RA were analyzed.Results: We identified 2670 cases of AKI events associated with GLP-1RA, of which liraglutide was the most commonly reported (34.98%). The patients with AKI were mainly males (47.94%), and the age group was mainly 45-84 years old (73.15%). obese patients with weight more than 99kg (24.42%) were more likely to have AKI. According to different signal mining methods, reporting odds ratio (ROR) (1.50, 95% confidence interval =1.41-1.60) and Bayesian confidence Propagation neural network (0.57, 95% confidence interval =0.54), liraglutide was more strongly associated with AKI than other GLP-1RA. The median time to onset of AKI was 63 days [quartile range (IQR): 15-458.5 days]. In addition, the hospitalization rate and fatality rate of patients with GLP-1RA-related AKI were 45.28% and 4.23% respectively.Conclusions: Based on the data in the FAERS database, we analyzed the risk, onset time, and adverse reaction outcomes of GLP-1RA-induced AKI in detail. The results showed that liraglutide had the highest risk of AKI. From the early stage of treatment, we need to monitor patients’ renal function regularly, especially for patients with high kidney risks such as obesity and age.

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, both in developed and developing countries. Despite the implementation of various measures in clinical practice that have shown certain curative effects, poor prognosis and irreversible pathological cardiac remodeling continue to limit the therapeutic effect of CVDs. There are still many new mechanisms worth exploring for the regulation of CVDs. Previous studies have highlighted the potential applicability of exosomes in CVDs, and significant research has been conducted in this area. In this review, we summarize the physiological mechanisms of exosomes and the basic research achievements in regulating CVDs via exosomal non-coding RNAs. We also discuss the limitations and prospects of exosome application in CVD treatment.