Modeling Kaempferol as a Potential Pharmacological Agent for COVID-19/PF Co-Occurrence Based on Bioinformatics and System Pharmacological Tools DOI Creative Commons
Yong Jiang,

Yizi Xie,

Chen-Wen Peng

et al.

Frontiers in Pharmacology, Journal Year: 2022, Volume and Issue: 13

Published: June 8, 2022

Objective: People suffering from coronavirus disease 2019 (COVID-19) are prone to develop pulmonary fibrosis (PF), but there is currently no definitive treatment for COVID-19/PF co-occurrence. Kaempferol with promising antiviral and anti-fibrotic effects expected become a potential COVID-19 PF comorbidities. Therefore, this study explored the targets molecular mechanisms of kaempferol against co-occurrence by bioinformatics network pharmacology. Methods: Various open-source databases Venn Diagram tool were applied confirm Protein-protein interaction (PPI), MCODE, key transcription factors, tissue-specific enrichment, docking, Gene ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) enrichment analyses used clarify influential Results: 290 203 factors captured. Epidermal growth factor receptor (EGFR), proto-oncogene tyrosine-protein kinase SRC (SRC), mitogen-activated protein 3 (MAPK3), 1 (MAPK1), 8 (MAPK8), RAC-alpha serine/threonine-protein (AKT1), p65 (RELA) phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA) identified as most critical targets, showed effective binding activities above eight targets. Further, anti-COVID-19/PF associated regulation inflammation, oxidative stress, immunity, virus infection, cell process metabolism. EGFR, interleukin 17 (IL-17), tumor necrosis (TNF), hypoxia inducible (HIF-1), phosphoinositide 3-kinase/AKT serine/threonine (PI3K/AKT) Toll-like signaling pathways pathways. Conclusion: candidate The underlying may be related (EGFR, SRC, MAPK3, MAPK1, MAPK8, AKT1, RELA, PIK3CA so on) IL-17, TNF, HIF-1, PI3K/AKT This contributes guiding development new drugs

Language: Английский

NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond DOI Creative Commons
Yuanfeng Zhu, Xiaoli Chen, Xin Liu

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: March 2, 2022

Infection with SARS-CoV-2, the causative agent of Coronavirus disease 2019 (COVID-19) pandemic, causes respiratory problems and multifaceted organ dysfunction. A crucial mechanism COVID-19 immunopathy is recruitment activation neutrophils at infection site, which also predicts severity poor outcomes. The release neutrophil extracellular traps (NETs), occurring during a regulated form cell death known as NETosis, key effector function that mediates harmful effects caused by neutrophils. Abundant NETosis NET generation have been observed in many patients, leading to unfavorable coagulopathy immunothrombosis. Moreover, excessive are now more widely recognized mediators additional pathophysiological abnormalities following SARS-CoV-2 infection. In this minireview, we introduce subtypes NET-producing (e.g., low-density granulocytes) explain biological importance NETs protein cargos COVID-19. addition, discuss mechanisms upregulating viral processes entry replication) well host pro-NET proinflammatory mediator release, platelet activation, autoantibody production). Furthermore, provide an update main findings immunothrombosis other COVID-19-related disorders, such aberrant immunity, neurological post syndromes including lung fibrosis, disorder, tumor progression, deteriorated chronic illness. Finally, address potential prospective treatment strategies target dysregulated formation via inhibition promotion degradation, respectively.

Language: Английский

Citations

136
Possible cancer-causing capacity of COVID-19: Is SARS-CoV-2 an oncogenic agent? DOI Open Access
Kasra Jahankhani,

Fatemeh Ahangari,

Ian M. Adcock

et al.

Biochimie, Journal Year: 2023, Volume and Issue: 213, P. 130 - 138

Published: May 23, 2023

Language: Английский

Citations

33
The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases DOI Creative Commons
Xiangguang Shi, Yahui Chen,

Mengkun Shi

et al.

Lipids in Health and Disease, Journal Year: 2024, Volume and Issue: 23(1)

Published: April 3, 2024

Abstract Pulmonary fibrosis (PF) is a severe pulmonary disease with limited available therapeutic choices. Recent evidence increasingly points to abnormal lipid metabolism as critical factor in PF pathogenesis. Our latest research identifies the dysregulation of low-density lipoprotein (LDL) new risk for PF, contributing alveolar epithelial and endothelial cell damage, fibroblast activation. In this study, we first integrative summarize published literature about metabolite changes found including phospholipids, glycolipids, steroids, fatty acids, triglycerides, lipoproteins. We then reanalyze two single-cell RNA-sequencing (scRNA-seq) datasets corresponding metabolomic genes responsible these lipids’ biosynthesis, catabolism, transport, modification processes are uncovered. Intriguingly, that macrophage most active type metabolism, almost all metabolic being altered macrophages PF. 2 cells, differentially expressed (DEGs) primarily associated cytidine diphosphate diacylglycerol pathway, cholesterol triglyceride synthesis. Endothelial cells partly sphingomyelin, phosphatidylcholine, phosphatidylethanolamines reprogramming their dysregulated Fibroblasts may contribute cholesterol, phosphatidylethanolamine Therefore, reprogrammed profiles be attributed aberrant expression different types. Taken together, insights underscore potential targeting developing innovative strategies, potentially leading extended overall survival individuals affected by

Language: Английский

Citations

9
SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis DOI
Anamika Gupta, Manju Nidagodu Jayakumar, Mohamed A. Saleh

et al.

Life Sciences, Journal Year: 2022, Volume and Issue: 304, P. 120703 - 120703

Published: June 11, 2022

Language: Английский

Citations

38
UHRF1-mediated ferroptosis promotes pulmonary fibrosis via epigenetic repression of GPX4 and FSP1 genes DOI Creative Commons
Yi Liu,

Demin Cheng,

Yue Wang

et al.

Cell Death and Disease, Journal Year: 2022, Volume and Issue: 13(12)

Published: Dec. 24, 2022

Abstract Pulmonary fibrosis (PF), as an end-stage clinical phenotype of interstitial lung diseases (ILDs), is frequently initiated after alveolar injury, in which ferroptosis has been identified a critical event aggravating the pathophysiological progression this disease. Here in, comprehensive analysis two mouse models pulmonary developed our lab demonstrated that damage-induced epithelial Type2 cells (AEC2) significantly accumulates during development while suppressor genes GPX4 and FSP1 are dramatically inactivated. Mechanistically, upregulation de novo methylation regulator Uhrf1 sensitively elevates CpG site levels promoters both induces epigenetic repression genes, subsequently leading to chemically interfered AEC2 cells. Meanwhile, specific inhibition UHRF1 highly arrests formation blocks research models. This study first, knowledge, involvement mediating injured AEC2s via promoter-specific consequently accelerates process fibrosis. The above findings also strongly suggested novel potential target treatment

Language: Английский

Citations

36
Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review DOI Creative Commons
Laura Bergantini,

Alessandro Mainardi,

Miriana d’Alessandro

et al.

Frontiers in Pharmacology, Journal Year: 2022, Volume and Issue: 13

Published: March 4, 2022

The pathogenetic mechanism of post-Covid-19 pulmonary fibrosis is currently a topic intense research interest, but still largely unexplored. aim this work was to carry out systematic exploratory search the literature (Scoping review) identify and systematize main mechanisms that are believed be involved in phenomenon, order highlight same molecular aspect lung. These aims could essential future for therapeutic management. We identified all primary studies involving post COVID19 syndrome with as endpoint by performing data searches various review databases. Two reviewers independently reviewed abstracts (398) full text data. quality study has been assess through SANRA protocol. A total 32 were included, included possible involvement inflammatory cytokines, concerned renin-angiotensin system, potential role galectin-3, epithelial injuries fibrosis, alveolar type 2 involvement, Neutrophil extracellular traps (NETs) others implied other specific aspects (relationship clinical mechanical factors, transition mesenchymal, TGF-β signaling pathway, midkine, caspase macrophages, genetics). In most cases, these narrative reviews or letters editor, except 10 articles, which presented original data, albeit sometimes experimental models. From development researches, progress knowledge phenomenon hopefully its prevention therapy may originate.

Language: Английский

Citations

31
Pulmonary fibrosis: A short- or long-term sequelae of severe COVID-19? DOI Creative Commons
Zhen Zheng, Fei Peng, Yong Zhou

et al.

Chinese Medical Journal - Pulmonary and Critical Care Medicine, Journal Year: 2023, Volume and Issue: 1(2), P. 77 - 83

Published: Jan. 23, 2023

The pandemic of coronavirus disease 2019 (COVID‑19), caused by a novel severe acute respiratory syndrome (SARS) 2 (SARS-CoV-2), has an enormous impact on the global healthcare. SARS-CoV-2 infection primarily targets system. Although most individuals testing positive for present mild or no upper tract symptoms, patients with COVID-19 can rapidly progress to distress (ARDS). ARDS-related pulmonary fibrosis is recognized sequelae COVID-19. Whether post-COVID-19 lung resolvable, persistent, even becomes progressive as seen in human idiopathic (IPF) currently not known and remains matter debate. With emergence effective vaccines treatments against COVID-19, it now important build our understanding long-term sequela infection, identify survivors who are at risk developing chronic fibrosis, develop anti-fibrotic therapies. current review aims summarize pathogenesis system highlights potential mechanisms. It envisions fibrotic complication survivors, particular aged population. early identification development therapies discussed.

Language: Английский

Citations

22
Hyaluronan in the pathogenesis of acute and post-acute COVID-19 infection DOI Open Access

Henry W. Barnes,

Sally Demirdjian, Naomi L. Haddock

et al.

Matrix Biology, Journal Year: 2023, Volume and Issue: 116, P. 49 - 66

Published: Feb. 1, 2023

Language: Английский

Citations

17
Antifibrotic Drugs against Idiopathic Pulmonary Fibrosis and Pulmonary Fibrosis Induced by COVID-19: Therapeutic Approaches and Potential Diagnostic Biomarkers DOI Open Access
Aurelio Perez-Favila, Idalia Garza‐Veloz,

Lucia del Socorro Hernandez-Marquez

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(3), P. 1562 - 1562

Published: Jan. 26, 2024

The COVID-19 pandemic has had a significant impact on the health and economy of global population. Even after recovery from disease, post-COVID-19 symptoms, such as pulmonary fibrosis, continue to be concern. This narrative review aims address fibrosis (PF) various perspectives, including fibrotic mechanisms involved in idiopathic COVID-19-induced fibrosis. On other hand, we also discuss current therapeutic drugs use, well those undergoing clinical or preclinical evaluation. Additionally, this article will biomarkers with usefulness for PF prediction, diagnosis, treatment, prognosis, severity assessment order provide better treatment strategies patients disease.

Language: Английский

Citations

8
Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 DOI Open Access
Daniela Adriana Oatis,

Erika Simon-Repolski,

Cornel Baltă

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(15), P. 8210 - 8210

Published: July 26, 2022

Pulmonary fibrosis is a consequence of the pathological accumulation extracellular matrix (ECM), which finally leads to lung scarring. Although pulmonary fibrogenesis almost known, last two years COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its post effects added new particularities need be explored. Many questions remain about how fibrotic changes occur within lungs patients, whether will persist long term or are capable resolving. This review brings together existing knowledge on both fibrosis, starting with main key players in promoting such as alveolar endothelial cells, fibroblasts, lipofibroblasts, macrophages. Further, we provide an overview molecular mechanisms driving process connection Galactin-1, -3, -8, -9, currently approved newly proposed clinical therapeutic solutions given for treatment based their inhibition. The work underlines particular pathways processes that may implicated pathogenesis post-SARS-CoV-2 viral infection. recent data suggest galectin-1, -9 could become valuable biomarkers diagnosis prognosis post-COVID-19 promising targets development original tools treat disease.

Language: Английский

Citations

23