Acute myocardial infarction (AMI) has the characteristics of sudden onset, rapid progression, poor prognosis, and so on. Therefore, it is urgent to identify diagnostic and prognostic biomarkers for it. Cuproptosis is a new form of mitochondrial respiratory-dependent cell death. However, studies are limited on the clinical significance of cuproptosis-related genes (CRGs) in AMI. In this study, we systematically assessed the genetic alterations of CRGs in AMI by bioinformatics approach. The results showed that six CRGs (LIAS, LIPT1, DLAT, PDHB, MTF1, and GLS) were markedly differentially expressed between stable coronary heart disease (stable_CAD) and AMI. Correlation analysis indicated that CRGs were closely correlated with N6-methyladenosine (m6A)-related genes through R language “corrplot” package, especially GLS was positively correlated with FMR1 and MTF1 was negatively correlated with HNRNPA2B1. Immune landscape analysis results revealed that CRGs were closely related to various immune cells, especially GLS was positively correlated with T cells CD4 memory resting and negatively correlated with monocytes. Kaplan–Meier analysis demonstrated that the group with high DLAT expression had a better prognosis. The area under curve (AUC) certified that GLS had good diagnostic value, in the training set (AUC = 0.87) and verification set (ACU = 0.99). Gene set enrichment analysis (GSEA) suggested that GLS was associated with immune- and hypoxia-related pathways. In addition, Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, competing endogenous RNA (ceRNA) analysis, transcription factor (TF), and compound prediction were performed to reveal the regulatory mechanism of CRGs in AMI. Overall, our study can provide additional information for understanding the role of CRGs in AMI, which may provide new insights into the identification of therapeutic targets for AMI.
Pyroptosis is a novel inflammatory form of regulated cell death (RCD), characterized by cell swelling, membrane rupture, and pro-inflammatory effects. It is recognized as a potent inflammatory response required for maintaining organismal homeostasis. However, excessive and persistent pyroptosis contributes to severe inflammatory responses and accelerates the progression of numerous inflammation-related disorders. In pyroptosis, activated inflammasomes cleave gasdermins (GSDMs) and generate membrane holes, releasing interleukin (IL)-1β/18, ultimately causing pyroptotic cell death. Mechanistically, pyroptosis is categorized into caspase-1-mediated classical pyroptotic pathway and caspase-4/5/11-mediated non-classical pyroptotic pathway. Renal fibrosis is a kidney disease characterized by the loss of structural and functional units, the proliferation of fibroblasts and myofibroblasts, and extracellular matrix (ECM) accumulation, which leads to interstitial fibrosis of the kidney tubules. Histologically, renal fibrosis is the terminal stage of chronic inflammatory kidney disease. Although there is a multitude of newly discovered information regarding pyroptosis, the regulatory roles of pyroptosis involved in renal fibrosis still need to be fully comprehended, and how to improve clinical outcomes remains obscure. Hence, this review systematically summarizes the novel findings regarding the role of pyroptosis in the pathogenesis of renal fibrosis and discusses potential biomarkers and drugs for anti-fibrotic therapeutic strategies.
Diabetic retinopathy (DR), a common and blinding diabetic microvascular complication, is a harmful metabolic effect caused by persistent hyperglycemia. Owing to the complex pathogenesis of DR, various clinical treatment methods cannot completely prevent its development and are accompanied by various complications. Therefore, there is an urgent need to identify new therapeutic drugs or complementary and alternative therapies. Traditional Chinese medicine (TCM) has the unique advantages of multi-level, multi-target, and minimal side effects. Accumulating evidence has proven that TCM may help delay or prevent the progression of DR. This paper reviews the effect and mechanism of representative TCMs (including extracts, identified compounds, and compound formulas) on DR in recent years and provides evidence for new drug development and clinical efficacy.
Review question / Objective: To investigate the efficacy of traditional Chinese medicine enema for pelvic inflammatory mass. The research method used was a RCT.
Purpose Diabetes has a common complication called diabetic peripheral neuropathy (DPN), whose exact pathophysiology is still unknown. In ischemic reperfusion injury to nerve tissues, the treatment of neurodegenerative illnesses, and the repair of nerve tissue injuries, autophagy is crucial. Through bioinformatics analysis and validation, we hope to pinpoint the possible autophagy-related differential expressed genes (DEGs) of DPN. Methods The GEO database provided the mRNA expression profile dataset GSE185011. R software was used to look for possible DPN autophagy-related DEGs. Then, for the autophagy-related DEGs, protein-protein interactions (PPI), correlation analysis, gene-ontology (GO) enrichment analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were carried out. In the validation set GSE95849, the RNA expression of autophagy-related DEGs was verified in blood samples from DPN patients and healthy controls. Results Between 5 DPN patients and 5 healthy controls, a total of 33 autophagy-related DEGs (5 up-regulated genes and 28 down-regulated genes) were found. The PPI analysis showed interactions between these autophagy-related DEGs. The GO and KEGG enrichment analyses revealed a number of enriched terms including mitophagy and autophagy. The results of the validation set demonstrated that the expression levels of the genes P4HB, GAPDH, CTSB and RAB7A were significantly decreased, ATG5, CASP3, SQSTM1, ULK1, and 9 other genes in DPN patients were significantly up-regulated in the DPN patients, which were compatible with the bioinformatics analysis of mRNA microarray. Conclusion Through bioinformatics research, we identified 17 putative autophagy-related DEGs in DPN. By regulating autophagy, ATG5, CASP3, SQSTM1, ULK1, and another 13 genes may have an impact on DPN formation. These findings might deepen our understanding of DPN and help with DPN treatment.
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