ArticleCellular and molecular life sciences : CMLS2022
Role of LL-37 in thrombotic complications in patients with COVID-19.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
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- Vitamin D-inducible antimicrobial peptide LL-37 binds SARS-CoV-2 Spike and accessory proteins ORF7a and ORF8.Frontiers in cellular and infection microbiology · 2025Article
- Peptides in wound healing: A comprehensive review of their roles, challenges, and hydrogel-based delivery systems.EXCLI journal · 2025Review
- Identifying potential co-expressed genes and molecular mechanisms linking post-COVID-19 and Guillain-Barre syndrome through neutrophil extracellular trap-related genes.Frontiers in neurology · 2025Article
- ShSPI Inhibits Thrombosis Formation and Ischemic Stroke In Vivo.International journal of molecular sciences · 2024Article
- The Impact of Cytokines on Coagulation Profile in COVID-19 Patients: Controlled for Socio-Demographic, Clinical, and Laboratory Parameters.Biomedicines · 2024Article
- Recent advances in the therapeutic potential of cathelicidins.Frontiers in microbiology · 2024Review
- Identification and Characterization of RK22, a Novel Antimicrobial Peptide fromInternational journal of molecular sciences · 2023Article
- The Coming of Age of the P2X7 Receptor in Diagnostic Medicine.International journal of molecular sciences · 2023Review
- NETs-Induced Thrombosis Impacts on Cardiovascular and Chronic Kidney Disease.Circulation research · 2023Review
- Novel mechanisms of thrombo-inflammation during infection: spotlight on neutrophil extracellular trap-mediated platelet activation.Research and practice in thrombosis and haemostasis · 2023Article
- Self-DNA driven inflammation in COVID-19 and after mRNA-based vaccination: lessons for non-COVID-19 pathologies.Frontiers in immunology · 2023Article
- Role of antimicrobial peptide cathelicidin in thrombosis and thromboinflammation.Frontiers in immunology · 2023Review
- The shed P2X7 receptor is an index of adverse clinical outcome in COVID-19 patients.Frontiers in immunology · 2023Article
- A designed antimicrobial peptide with potential ability against methicillin resistantFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Blood clot formation induced by dysfunctional coagulation is a frequent complication of coronavirus disease 2019 (COVID-19) and a high-risk factor for severe illness and death. Neutrophil extracellular traps (NETs) are implicated in COVID-19-induced immunothrombosis. Furthermore, human cathelicidin, a NET component, can perturb the interaction between the SARS-CoV-2 spike protein and its ACE2 receptor, which mediates viral entry into cells. At present, however, the levels of cathelicidin antimicrobial peptides after SARS-CoV-2 infection and their role in COVID-19 thrombosis formation remain unclear. In the current study, we analyzed coagulation function and found a decrease in thrombin time but an increase in fibrinogen level, prothrombin time, and activated partial thromboplastin time in COVID-19 patients. In addition, the cathelicidin antimicrobial peptide LL-37 was upregulated by the spike protein and significantly elevated in the plasma of patients. Furthermore, LL-37 levels were negatively correlated with thrombin time but positively correlated with fibrinogen level. In addition to platelet activation, cathelicidin peptides enhanced the activity of coagulation factors, such as factor Xa (FXa) and thrombin, which may induce hypercoagulation in diseases with high cathelicidin peptide levels. Injection of cathelicidin peptides promoted the formation of thrombosis, whereas deletion of cathelicidin inhibited thrombosis in vivo. These results suggest that cathelicidin antimicrobial peptide LL-37 is elevated during SARS-CoV-2 infection, which may induce hypercoagulation in COVID-19 patients by activating coagulation factors.
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