Transcriptomic Hallmarks of Ischemia-Reperfusion Injury.
Mandana MovahedSydney BrockieJames HongMichael G FehlingsPublished in: Cells (2021)
Ischemia reperfusion injury (IRI) is associated with a broad array of life-threatening medical conditions including myocardial infarct, cerebral stroke, and organ transplant. Although the pathobiology and clinical manifestations of IRI are well reviewed by previous publications, IRI-related transcriptomic alterations are less studied. This study aimed to reveal a transcriptomic hallmark for IRI by using the RNA-sequencing data provided by several studies on non-human preclinical experimental models. In this regard, we focused on the transcriptional responses of IRI in an acute time-point up to 48 h. We compiled a list of highly reported genes in the current literature that are affected in the context of IRI. We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses and found many of the up-regulated genes to be involved in cell survival, cell surface signaling, response to oxidative stress, and inflammatory response, while down-regulated genes were predominantly involved in ion transport. Furthermore, by GO analysis, we found that multiple inflammatory and stress response processes were affected after IRI. Tumor necrosis factor alpha (TNF) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways were also highlighted in the Kyoto Encyclopedia of Genes and Genomes enrichment analysis. In the last section, we discuss the treatment approaches and their efficacy for IRI by comparing RNA sequencing data from therapeutic interventions with the results of our cross-comparison of differentially expressed genes and pathways across IRI.
Keyphrases
- genome wide
- nuclear factor
- oxidative stress
- single cell
- genome wide identification
- ischemia reperfusion injury
- transcription factor
- inflammatory response
- bioinformatics analysis
- signaling pathway
- genome wide analysis
- rna seq
- dna methylation
- healthcare
- rheumatoid arthritis
- systematic review
- gene expression
- dna damage
- left ventricular
- stem cells
- acute myocardial infarction
- high throughput
- cell surface
- big data
- copy number
- electronic health record
- induced apoptosis
- lps induced
- high resolution
- epithelial mesenchymal transition
- cell proliferation
- immune response
- respiratory failure
- pi k akt
- mass spectrometry
- deep learning
- acute respiratory distress syndrome
- acute coronary syndrome
- extracorporeal membrane oxygenation
- liver failure
- induced pluripotent stem cells
- coronary artery disease