ReviewFrontiers in immunology2024
Multifaceted role of SARS-CoV-2 structural proteins in lung injury.
Review in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Cellular and Molecular Mechanisms of SARS-CoV-2 Spike Protein-Induced Endothelial Dysfunction.Cells · 2026Review
- MiR-24 Attenuates Oxidative Stress and Mitochondrial Apoptosis in Ventilator-Induced Lung Injury by Targeting Bcl-2-related Ovarian Killer.Pulmonary circulation · 2025Article
- The ACE2 decoy receptor can overcome immune escape by rapid mutating SARS-CoV-2 variants and reduce cytokine induction and clot formation.Journal of biomedical science · 2025Article
- Risk impact of SARS-CoV-2 coronavirus and spike protein on cardiac tissue: a comprehensive review.Physiological research · 2024Review
- Quantitative IgG response to SARS-CoV-2 membrane protein in infected individuals strongly correlates with lung injury.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third human coronavirus to cause acute respiratory distress syndrome (ARDS) and contains four structural proteins: spike, envelope, membrane, and nucleocapsid. An increasing number of studies have demonstrated that all four structural proteins of SARS-CoV-2 are capable of causing lung injury, even without the presence of intact virus. Therefore, the topic of SARS-CoV-2 structural protein-evoked lung injury warrants more attention. In the current article, we first synopsize the structural features of SARS-CoV-2 structural proteins. Second, we discuss the mechanisms for structural protein-induced inflammatory responses
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