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pmid:38295140
Transcriptome and machine learning analysis of the impact of COVID-19 on mitochondria and multiorgan damage.
Yu-Yu Chang · An-Chi Wei
PloS one · 2024 doi:10.1371/journal.pone.0297664
Paper
complete
Experiment
complete
Data
partial
Analysis
complete
Execution
absent
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Complete file
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COVID-19 may involve multiorgan damage from direct viral invasion through angiotensin-converting enzyme 2 (ACE2), through inflammatory cytokine storms, or through other secondary pathways. This study involved the analysis of publicly accessible transcriptome data from the Gene Expression Omnibus (GEO) database for identifying significant differentially expressed genes related to COVID-19 and an investigation relating to the pathways associated with mitochondrial, cardiac, hepatic, and renal toxicity in COVID-19. Significant differentially expressed genes were identified and ranked by statistical approaches, and the genes derived by biological meaning were ranked by feature importance; both were utilized as machine learning features for verification. Sample set selection for machine learning was based on the performance, sample size, imbalanced data state, and overfitting assessment. 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NetworkAn", "tissue specific. The common genes across the RNA-seq datasets.Top 100 significantly expressed gen"], "order_basis": "paper_text_order:0", "id": "assay:1"}, {"role": "data_generation", "definition_id": "apoptosis_assay", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["a proapoptotic member involved in initiating apoptosis, which might explain the cell death in vario", "le damage to cellular components and trigger apoptosis through the mitochondrial intrinsic apoptoti", "[60]. Therefore, oxidative stress can cause apoptosis via a mitochondria-dependent pathway [61]. 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