ABSTRACT
【Objective】 To make bioinformatics analysis of inflammatory cardiomyopathy so as to screen out hub genes related to etiology and therapeutic targets. 【Methods】 Differential expression analysis of inflammatory cardiomyopathy gene chip data from Gene Expression Omnibus （GEO） Database was carried out via GEO2R tool. Protein-protein interaction（PPI）network and hub genes identification were realized by String database and CytoHubba. GO and KEGG enrichment analysis for functional annotation and pathway analysis of hub genes were conducted by R language. Web-based enrichment analysis platform Enrichr and Drug Signatures database were applied to screen out candidate drugs targeting hub genes for inflammatory cardiomyopathy. 【Results】 The 149 DEGs were statistically significant， among which 44 were upregulated and 105 were downregulated. To identify hub genes， PPI network consisting of 37 nodes and 116 edges was constructed， and 16 hub genes were NDUFB7， POLR2L， NDUFS7， UQCR11， NDUFA13， NDUFA2， PHPT1， NDUFB10， UBA52， ATP5D， NDUFA3， COX6B1， POLR2J， COX4I2， AURKAIP1 and MRPL41. Hub genes were enriched to 113 different GO terms， and the most significant terms were mitochondrial ATP synthesis coupled electron transport， respiratory electron transport chain， oxidative phosphorylation， respiratory chain， mitochondrial inner membrane， NADH dehydrogenase activity and oxidoreductase activity. DEGs were enriched to 13 different signal pathways， including oxidative phosphorylation， non-alcoholic fatty liver disease， diabetic cardiomyopathy， and cardiac muscle contraction. We screened out candidate drugs targeting hub genes， namely， metformin hydrochloride， clindamycin， and hydralazine. 【Conclusion】 Hub genes screened out by decoding the expression profiles are convolved in the etiology and mechanism of inflammatory cardiomyopathy， which might serve as latent therapeutic targets and benefit patients with inflammatory cardiomyopathy.
ABSTRACT
Background: Role of immunosuppression treatment in patients with inflammatory dilated cardiomyopathy is controversial. The aim of this review is to summarize current evidence for immunosuppressive therapy in inflammatory cardiomyopathy. Methods: A systematic literature search was performed using PubMed, Embase and MELDINE to identify trials comparing immunosuppressive therapy with either placebo or conventional medical therapy in adult patients with inflammatory cardiomyopathy. Combined primary outcome in our study was all cause mortality and heart transplantation. Secondary outcomes included improvement in left ventricular ejection fraction (LVEF) and left ventricular end diastolic dimension (LVEDD). Results: Five randomized controlled trials (RCTs) were identified and four trials with similar comparable groups, with a total of 359 adult patients were included for analysis. Pooled data demonstrated no reduction in all-cause mortality and heart transplantation amongst the immunosuppression or the placebo arm (OR 0.98, 95% CI 0.48-1.98). There was a significant improvement in LVEF (1.34%, 95% CI 0.37-2.30) in patients treated with immunosuppressive medications, however no difference was observed in LVEDD [-0.11mm (95% CI -1.92 – 1.71)] in the treatment arm. Conclusion: There was no survival benefit or reduction in heart transplantation events with a significant improvement in LVEF in inflammatory cardiomyopathy patients treated with immunosuppression therapy.
ABSTRACT
Viral myocarditis can cause severe myocardial injury and even acute heart failure, then evolve into dilated cardiomyopathy, known as inflammatory cardiomyopathy. Immune reaction plays a key role in the transformation from viral myocarditis into dilated cardiomyopathy, including virus RNA continuous replication,immune-mediated injury, cellular apoptosis, other cellular immune response , myocardial antibodies and other humoral immune response. In the clinical treatment, besides anti-heart failure and cardiac nutrition, the use of ribavirin, α1-receptor blockers, β-receptor blockers, calcium channel blockers, angiotensin converting enzyme inhibitors and spironolactone should be emphasized.