ArticleFrontiers in physiology2022
HSP90 Inhibitors Modulate SARS-CoV-2 Spike Protein Subunit 1-Induced Human Pulmonary Microvascular Endothelial Activation and Barrier Dysfunction.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- T1R3 Anchors ACE2 at the Pulmonary Endothelial Cell Surface to Attenuate Vascular Injury Following SARS-CoV-2 Spike 1 Protein Exposure In Vitro.Journal of cellular and molecular medicine · 2026Article
- Combination therapy with HSP90 inhibitors and NanoPulse stimulation synergistically impedes hepatocellular carcinoma and breast cancer growth in mice.Scientific reports · 2026Article
- Acute lung injury induced by recombinant SARS-CoV-2 spike protein subunit S1 in mice.Respiratory research · 2025Article
- The role of heat shock protein 90 in idiopathic pulmonary fibrosis: state of the art.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Influenza, SARS-CoV-2, and Their Impact on Chronic Lung Diseases and Fibrosis: Exploring Therapeutic Options.The American journal of pathology · 2024Review
- Protective role of the HSP90 inhibitor, STA-9090, in lungs of SARS-CoV-2-infected Syrian golden hamsters.BMJ open respiratory research · 2024Article
- Review
- The SARS-CoV-2 spike S1 protein induces global proteomic changes in ATII-like rat L2 cells that are attenuated by hyaluronan.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- COVID-19 Vaccination and Alcohol Consumption: Justification of Risks.Pathogens (Basel, Switzerland) · 2023Review
- Label-Free Analysis of Binding and Inhibition of SARS-Cov-19 Spike Proteins to ACE2 Receptor with ACE2-Derived Peptides by Surface Plasmon Resonance.ACS applied bio materials · 2023Article
- Heat shock protein 90 inhibition in the endothelium.Frontiers in medicine · 2023Article
- Syphilis and the host: multi-omic analysis of host cellular responses toFrontiers in microbiology · 2023Article
- SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF-β signaling.Nature communications · 2022Article
- Calcium dobesilate reduces SARS-CoV-2 entry into endothelial cells by inhibiting virus binding to heparan sulfate.Scientific reports · 2022Article
- The Role of Nuclear Factor Kappa B (NF-κB) in Development and Treatment of COVID-19: Review.International journal of molecular sciences · 2022Review
- Endothelial cell-derived extracellular vesicles impair the angiogenic response of coronary artery endothelial cells.Frontiers in cardiovascular medicine · 2022Article
- The role of angiotensin I converting enzyme insertion/deletion polymorphism in the severity and outcomes of COVID-19 patients.Frontiers in genetics · 2022Article
- Optimizing antidotal treatment with the oral HSP90 inhibitor TAS-116 against hydrochloric acid-induced pulmonary fibrosis in mice.Frontiers in pharmacology · 2022Article
- Host cell stress response as a predictor of COVID-19 infectivity and disease progression.Frontiers in molecular biosciences · 2022Review
- Targeting heat shock proteins 90 and 70: A promising remedy for both autoimmune bullous diseases and COVID-19.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused more than 5 million deaths worldwide. Multiple reports indicate that the endothelium is involved during SARS-Cov-2-related disease (COVID-19). Indeed, COVID-19 patients display increased thrombophilia with arterial and venous embolism and lung microcapillary thrombotic disease as major determinants of deaths. The pathophysiology of endothelial dysfunction in COVID-19 is not completely understood. We have investigated the role of subunit 1 of the SARS-CoV-2 spike protein (S1SP) in eliciting endothelial barrier dysfunction, characterized dose and time relationships, and tested the hypothesis that heat shock protein 90 (HSP90) inhibitors would prevent and repair such injury. S1SP activated (phosphorylated) IKBα, STAT3, and AKT and reduced the expression of intercellular junctional proteins, occludin, and VE-cadherin. HSP90 inhibitors (AT13387 and AUY-922) prevented endothelial barrier dysfunction and hyperpermeability and reduced IKBα and AKT activation. These two inhibitors also blocked S1SP-mediated barrier dysfunction and loss of VE-cadherin. These data suggest that spike protein subunit 1 can elicit, by itself, direct injury to the endothelium and suggest a role of HSP90 inhibitors in preserving endothelial functionality.
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