ArticleJournal of translational medicine2023
Landscape of molecular crosstalk between SARS-CoV-2 infection and cardiovascular diseases: emphasis on mitochondrial dysfunction and immune-inflammation.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting GLS and LPIN2 in renal fibroblasts: potential therapeutic targets for kidney stone disease identified by integrated multi-omics analysis.Urolithiasis · 2026Article
- Modulation of mitochondrial dysfunction: Mechanisms and strategies for the use of natural products to treat stroke.Neural regeneration research · 2026Article
- Uncovering G Protein-Coupled Receptors: Novel Targets and Biomarkers for Predicting Glioma Prognosis.Annals of clinical and translational neurology · 2026Article
- Potential causal role of mitochondrial biological effects in COVID-19: Evidence from Mendelian randomization study.Medicine · 2026Article
- SARS-CoV-2 damages cardiomyocyte mitochondria and implicates long COVID-associated cardiovascular manifestations.Journal of advanced research · 2026Article
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
- Integrated bioinformatics analysis to develop diagnostic models for malignant transformation of chronic proliferative diseases.Blood science (Baltimore, Md.) · 2025Article
- Inhibition of kinin B1 receptor alleviates SARS-CoV-2-induced long-lasting cardiovascular complications.American journal of physiology. Heart and circulatory physiology · 2025Article
- Relationship between preoperative high arterial blood lactate level and delirium after deep brain stimulation surgery in Parkinson's disease.Frontiers in aging · 2025Article
- Alterations in microbiota of patients with COVID-19: implications for therapeutic interventions.MedComm · 2024Review
- Post COVID-19 Reflections and Questions: How Prepared Are We for the Next Pandemic?International journal of molecular sciences · 2024Article
- Exploring the common mechanism of vascular dementia and inflammatory bowel disease: a bioinformatics-based study.Frontiers in immunology · 2024Article
- Weighted gene co-expression network analysis and whole genome sequencing identify potential lung cancer biomarkers.Frontiers in oncology · 2024Article
- Aging mitochondria in the context of SARS-CoV-2: exploring interactions and implications.Frontiers in aging · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSARS-CoV-2, the pathogen of COVID-19, is a worldwide threat to human health and causes a long-term burden on the cardiovascular system. Individuals with pre-existing cardiovascular diseases are at higher risk for SARS-CoV-2 infection and tend to have a worse prognosis. However, the relevance and pathogenic mechanisms between COVID-19 and cardiovascular diseases are not yet completely comprehended.
methodsCommon differentially expressed genes (DEGs) were obtained in datasets of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) infected with SARS-CoV-2 and myocardial tissues from heart failure patients. Further GO and KEGG pathway analysis, protein-protein interaction (PPI) network construction, hub genes identification, immune microenvironment analysis, and drug candidate predication were performed. Then, an isoproterenol-stimulated myocardial hypertrophy cell model and a transverse aortic constriction-induced mouse heart failure model were employed to validate the expression of hub genes.
resultsA total of 315 up-regulated and 78 down-regulated common DEGs were identified. Functional enrichment analysis revealed mitochondrial metabolic disorders and extensive immune inflammation as the most prominent shared features of COVID-19 and cardiovascular diseases. Then, hub DEGs, as well as hub immune-related and mitochondria-related DEGs, were screened. Additionally, nine potential therapeutic agents for COVID-19-related cardiovascular diseases were proposed. Furthermore, the expression patterns of most of the hub genes related to cardiovascular diseases in the validation dataset along with cellular and mouse myocardial damage models, were consistent with the findings of bioinformatics analysis.
conclusionsThe study unveiled the molecular networks and signaling pathways connecting COVID-19 and cardiovascular diseases, which may provide novel targets for intervention of COVID-19-related cardiovascular diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.