RÉSUMÉ
BACKGROUND: Treatment-resistant depression (TRD) is a condition in a subset of depressed patients characterized by resistance to antidepressant medications. The global prevalence of TRD has been steadily increasing, yet significant advancements in its diagnosis and treatment remain elusive despite extensive research efforts. The precise underlying pathogenic mechanisms are still not fully understood. Epigenetic mechanisms play a vital role in a wide range of diseases. In recent years, investigators have increasingly focused on the regulatory roles of miRNAs in the onset and progression of TRD. miRNAs are a class of noncoding RNA molecules that regulate the translation and degradation of their target mRNAs via interaction, making the exploration of their functions in TRD essential for elucidating their pathogenic mechanisms. METHODS AND RESULTS: A systematic search was conducted in four databases, namely PubMed, Web of Science, Cochrane Library, and Embase, focusing on studies related to treatment-resistant depression and miRNAs. The search was performed using terms individually or in combination, such as "treatment-resistant depression," "medication-resistant depression," and "miRNAs." The selected articles were reviewed and collated, covering the time period from the inception of each database to the end of February 2024. We found that miRNAs play a crucial role in the pathophysiology of TRD through three main aspects: 1) involvement in miRNA-mediated inflammatory responses (including miR-155, miR-345-5p, miR-146a, and miR-146a-5p); 2) influence on 5-HT transport processes (including miR-674,miR-708, and miR-133a); and 3) regulation of synaptic plasticity (including has-miR-335-5p,has-miR- 1292-3p, let-7b, and let-7c). Investigating the differential expression and interactions of these miRNAs could contribute to a deeper understanding of the molecular mechanisms underlying TRD. CONCLUSIONS: miRNAs might play a pivotal role in the pathogenesis of TRD. Gaining a deeper understanding of the roles and interrelations of miRNAs in TRD will contribute to elucidating disease pathogenesis and potentially provide avenues for the development of novel diagnostic and therapeutic strategies.
Sujet(s)
Trouble dépressif résistant aux traitements , microARN , Humains , microARN/génétique , Trouble dépressif résistant aux traitements/génétique , Trouble dépressif résistant aux traitements/thérapie , Antidépresseurs/usage thérapeutique , Antidépresseurs/pharmacologie , Régulation de l'expression des gènes , Épigenèse génétiqueRÉSUMÉ
OBJECTIVE: To explore gut microbiota changes in intractable epilepsy patients compared to healthy control individuals through meta-analysis. METHODS: PubMed, Web of Science, CNKI, Wanfang, medRxiv, bioRxiv, ilae.org, clinical trial databases, and papers from the International Epilepsy Congress (IEC) were searched, and the literature on the correlation between intractable epilepsy and the gut microbiota reported from database establishment to June 2023 was included. Literature meeting the inclusion criteria was screened, and meta-analysis of the included literature was performed using RevMan5.4 software. RESULTS: Ten case-control studies were included in the meta-analysis. There were 183 patients with intractable epilepsy and 283 healthy control subjects. The analysis results indicated that Bacteroidetes (MD = -0.64, 95 %-CI = -1.21 to -0.06) and Ruminococcaceae (MD = -1.44, 95 % CI = -1.96 to -0.92) were less abundant in the patients with intractable epilepsy than in the normal population. Proteobacteria (MD = 0.53, 95 % CI = 0.02 to 1.05) and Verrucomicrobia (MD = 0.26, 95 % CI = 0.06 to 0.45) were more abundant in the patients with intractable epilepsy than in the normal population. CONCLUSION: This meta-analysis indicated that the abundances of Bacteroidetes and Ruminococcaceae were reduced while those of Proteobacteria and Verrucomicrobia were significantly increased in patients with intractable epilepsy. The above changes in these four taxa of the gut microbiota may have been induced by intractable epilepsy, which may increase the risk of seizures. Their roles in the pathogenesis of intractable epilepsy need to be further explored, and related factors that influence microbiota changes should be considered in future studies.
Sujet(s)
Épilepsie pharmacorésistante , Microbiome gastro-intestinal , Humains , Crises épileptiques , Études cas-témoins , Bases de données factuellesRÉSUMÉ
Background: Numerous parallels exist between inflammatory bowel disease (IBD) and allergic rhinitis (AR), which include risk factors (such as environmental and genetic factors), pathogenesis (immune disorders, epithelial cell barriers, etc.), and treatment (immunosuppressants and immunomodulators, such as cyclosporine and steroids). However, the risk of AR in IBD patients is unknown. Objective: In this systematic review and meta-analysis, patients with IBD are examined for their risk of AR. Methods: Several databases are accessible in both Chinese and English, including PubMed, BioRXiv, WanFang, the China National Knowledge Infrastructure (CNKI), Web of Science, METSTR, and MedRxiv. Findings presented at allergy, rhinology, thoracic, and gastrointestinal conferences were analyzed. Based on the inclusion and exclusion criteria, two evaluators independently retrieved data, read the literature, and evaluated bias risk. The data analysis was conducted using RevMan 5.4. Case-control and cohort studies were eligible study designs for this research. Results: There were 10 case-control studies and 1 cohort study included in the meta-analysis. The experimental group consisted of 65,687 IBD patients, of whom 5838 had AR. A total of 345,176 participants without IBD were included in the control group, of whom 24,625 developed AR. The outcomes demonstrated that IBD patients had a higher risk of developing AR (odds ratio [OR] = 1.48, 95% confidence interval [CI] [1.12, 1.95], Z = 2.78, P = 0.005) than those without IBD. Conclusion: The risk of AR is higher in IBD patients. Further investigation is required to determine the mechanism behind the association between AR and IBD (AU)