Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313503104> ?p ?o ?g. }
- W4313503104 abstract "Sepsis is a life-threatening organ dysfunction caused by dysregulated host immune response to infection. Sepsis-induced myocardial dysfunction (SIMD) is a common complication in patients with severe sepsis and is associated with increased mortality. The molecular mechanisms underlying SIMD are complex and not well characterized. Excessive inflammation due to impaired regulation of immune response is one of the major causes of SIMD. Necroptosis is a novel type of cell death that is closely related to tissue injury and inflammation. However, the role of necroptosis in SIMD is not known. Therefore, in this study, we performed an in-depth bioinformatics analysis to investigate the relationship between necroptosis and SIMD using a mouse model generated by intraperitoneal injection of lipopolysaccharide (LPS) and the underlying mechanisms. Myocardial function was assessed by echocardiography. Histopathological changes in SIMD were analyzed by hematoxylin and eosin (H&E) staining. Gene expression profiles of the heart tissues from the SIMD and control mice were analyzed by bioinformatics analysis. Transcriptome sequencing demonstrated significant differences in the expression levels of 3654 genes in the heart tissues of SIMD mice including 1810 up-regulated and 1844 down-regulated genes. The necroptosis pathway genes were significantly enriched in the heart tissues from the SIMD group mice. We identified 35 necroptosis-related differentially expressed genes (NRDEGs) including MLKL and RIPK3. Cardiomyocyte necroptosis was confirmed by qRT-PCR and western blot analysis. The expression levels of most NRDEGs showed positive correlation with the infiltration levels of mast cells, macrophages, and neutrophils, and negative correlation with the infiltration levels of B cells and plasma cells in the heart tissues of the SIMD group mice. In conclusion, this study demonstrated that necroptosis was associated with changes in the infiltration levels of several immune cell types in the heart tissues of the SIMD model mice. This suggested that necroptosis influenced SIMD development by modulating the immune microenvironment. This suggested that NRDEGs are potential diagnostic biomarkers and therapeutic targets for patients with SIMD." @default.
- W4313503104 created "2023-01-06" @default.
- W4313503104 creator A5008713080 @default.
- W4313503104 creator A5010282117 @default.
- W4313503104 creator A5014924965 @default.
- W4313503104 creator A5021379796 @default.
- W4313503104 creator A5030107320 @default.
- W4313503104 creator A5052441498 @default.
- W4313503104 creator A5074779366 @default.
- W4313503104 date "2022-12-21" @default.
- W4313503104 modified "2023-09-30" @default.
- W4313503104 title "New insights of necroptosis and immune infiltration in sepsis-induced myocardial dysfunction from bioinformatics analysis through RNA-seq in mice" @default.
- W4313503104 cites W1882905539 @default.
- W4313503104 cites W1974285357 @default.
- W4313503104 cites W1985987855 @default.
- W4313503104 cites W1991027668 @default.
- W4313503104 cites W1991593801 @default.
- W4313503104 cites W2008961838 @default.
- W4313503104 cites W2017534273 @default.
- W4313503104 cites W2021608460 @default.
- W4313503104 cites W2032227357 @default.
- W4313503104 cites W2047998870 @default.
- W4313503104 cites W2068619092 @default.
- W4313503104 cites W2076080662 @default.
- W4313503104 cites W2096173332 @default.
- W4313503104 cites W2097476575 @default.
- W4313503104 cites W2130410032 @default.
- W4313503104 cites W2134678519 @default.
- W4313503104 cites W2137531873 @default.
- W4313503104 cites W2139552156 @default.
- W4313503104 cites W2141738274 @default.
- W4313503104 cites W2146512944 @default.
- W4313503104 cites W2280404143 @default.
- W4313503104 cites W2511592035 @default.
- W4313503104 cites W2520610051 @default.
- W4313503104 cites W2527488980 @default.
- W4313503104 cites W2540365220 @default.
- W4313503104 cites W2596265142 @default.
- W4313503104 cites W2751150663 @default.
- W4313503104 cites W2774868879 @default.
- W4313503104 cites W2782135811 @default.
- W4313503104 cites W2788142646 @default.
- W4313503104 cites W2790646472 @default.
- W4313503104 cites W2804721740 @default.
- W4313503104 cites W2805299785 @default.
- W4313503104 cites W2806162384 @default.
- W4313503104 cites W2888777689 @default.
- W4313503104 cites W2889367571 @default.
- W4313503104 cites W2890862843 @default.
- W4313503104 cites W2890977746 @default.
- W4313503104 cites W2897087128 @default.
- W4313503104 cites W2897675687 @default.
- W4313503104 cites W2901410206 @default.
- W4313503104 cites W2901715240 @default.
- W4313503104 cites W2914524806 @default.
- W4313503104 cites W2938247032 @default.
- W4313503104 cites W2942035615 @default.
- W4313503104 cites W2945777288 @default.
- W4313503104 cites W2946044964 @default.
- W4313503104 cites W2946057803 @default.
- W4313503104 cites W2965244259 @default.
- W4313503104 cites W2974507609 @default.
- W4313503104 cites W3021834206 @default.
- W4313503104 cites W3093872367 @default.
- W4313503104 cites W3153983509 @default.
- W4313503104 cites W3185587603 @default.
- W4313503104 cites W3186053696 @default.
- W4313503104 cites W3197034218 @default.
- W4313503104 cites W3206455119 @default.
- W4313503104 cites W3216414161 @default.
- W4313503104 cites W4200499622 @default.
- W4313503104 cites W4242587027 @default.
- W4313503104 cites W94556339 @default.
- W4313503104 doi "https://doi.org/10.3389/fcimb.2022.1068324" @default.
- W4313503104 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36619743" @default.
- W4313503104 hasPublicationYear "2022" @default.
- W4313503104 type Work @default.
- W4313503104 citedByCount "0" @default.
- W4313503104 crossrefType "journal-article" @default.
- W4313503104 hasAuthorship W4313503104A5008713080 @default.
- W4313503104 hasAuthorship W4313503104A5010282117 @default.
- W4313503104 hasAuthorship W4313503104A5014924965 @default.
- W4313503104 hasAuthorship W4313503104A5021379796 @default.
- W4313503104 hasAuthorship W4313503104A5030107320 @default.
- W4313503104 hasAuthorship W4313503104A5052441498 @default.
- W4313503104 hasAuthorship W4313503104A5074779366 @default.
- W4313503104 hasBestOaLocation W43135031041 @default.
- W4313503104 hasConcept C104317684 @default.
- W4313503104 hasConcept C150194340 @default.
- W4313503104 hasConcept C150552126 @default.
- W4313503104 hasConcept C162317418 @default.
- W4313503104 hasConcept C173608175 @default.
- W4313503104 hasConcept C190283241 @default.
- W4313503104 hasConcept C203014093 @default.
- W4313503104 hasConcept C2776914184 @default.
- W4313503104 hasConcept C2778384902 @default.
- W4313503104 hasConcept C2780942790 @default.
- W4313503104 hasConcept C31573885 @default.
- W4313503104 hasConcept C41008148 @default.
- W4313503104 hasConcept C502942594 @default.