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Interplay Between Coagulation and Inflammation: Molecular Mechanisms, Clinical Implications, and Therapeutic Strategies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 June 2025) | Viewed by 1161

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Guest Editor
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA
Interests: endothelial inflammation; endothelial permeability; vascular remodeling
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Special Issue Information

Dear Colleagues,

The common factor underlying many illnesses affecting the cardiovascular system is the interaction between inflammation and coagulation. Under normal circumstances, the equilibrium between anticoagulants and coagulants and anti-inflammatory and inflammatory pathways preserves homeostasis. In a diseased state, the body’s response to infection or injury leads to the activation of the coagulation and inflammation cascade, commonly referred to as immunothrombosis. However, excessive and unregulated immunothrombosis responses cause catastrophic damage that compromises organ functions, also known as thromboinflammation. Thromboinflammation is especially relevant to COVID-19 since the virus causes enhanced inflammation and coagulation responses in infected patients. The natural anticoagulants such as thrombomodulin, anti-thrombin, and activated protein C facilitate the neutralization of some inflammatory mediators and increase the endothelial barrier function. Hence, the downregulation of anticoagulant pathways not only promotes thrombosis but also amplifies the inflammatory process. Thus, elucidating the role of inflammation in coagulation and vice versa will introduce new perspectives to improve clinical diagnostics and therapeutic strategies for the future, leading to improved patient care. 

We welcome original research articles, reviews, or shorter perspective articles on all aspects related to the coagulation and inflammation processes. Articles with mechanistic insights from cellular and molecular perspectives are especially welcome. Some of the relevant topics include, but are not limited to, the following: thromboinflammation in COVID-19; thromboinflammation and oxidative stress; thromboinflammation and aging; the role of extracellular vesicle biology in thromboinflammation; thromboinflammation affecting the cognitive functions of brain and visual acuity; and thromboinflammation affecting vascular and tissue remodeling.

Dr. Hemant Giri
Guest Editor

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Keywords

  • coagulation
  • inflammation
  • endothelial dysfunction
  • anticoagulants
  • inflammation
  • venous thrombosis
  • venous thromboembolism
  • thromboinflammation
  • coagulation
  • inflammasomes
  • neutrophil extracellular traps
  • platelets
  • endothelial activation
  • vascular remodeling

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Published Papers (2 papers)

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Research

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13 pages, 260 KiB  
Article
Extracellular Vesicles Profile and Risk of Venous Thromboembolism in Patients with Diffuse Large B-Cell Lymphoma
by Vladimir Otasevic, Charlotte Gran, Natasa Milic, Jelena Ivanovic, Sofija Kozarac, Vojin Vukovic, Biljana Mihaljevic, Nikolina Dukic, Jelena Vladicic Masic, Jawed Fareed, Jovan Antovic and Darko Antic
Int. J. Mol. Sci. 2025, 26(12), 5655; https://doi.org/10.3390/ijms26125655 - 12 Jun 2025
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Abstract
Thrombosis is a common complication in cancer patients, with a substantial impact on morbidity and mortality. Diffuse large B-cell lymphoma (DLBCL) and other aggressive lymphomas carry a high venous thromboembolism (VTE) risk. Extracellular vesicles (EVs) have gained attention in recent research as a [...] Read more.
Thrombosis is a common complication in cancer patients, with a substantial impact on morbidity and mortality. Diffuse large B-cell lymphoma (DLBCL) and other aggressive lymphomas carry a high venous thromboembolism (VTE) risk. Extracellular vesicles (EVs) have gained attention in recent research as a new potential biomarker for VTE development. To determine the profile and association of EVs with VTE in patients with DLBCL, we conducted a prospective cohort study on 62 patients diagnosed with DLBCL. A total of 11 patients (17.7%) developed VTE. The concentrations of platelet-derived EVs (PEVs), E-selectin+ EVs, P-selectin+ EVs, tissue factor (TF)-positive/CD20+ EVs, TF−/CD19+ EVs, TF−/CD45+ EVs, and TF−/CD20+ EVs were significantly higher in DLBCL patients compared to healthy controls. In contrast, the concentration of TF− PEVs was significantly lower in DLBCL patients compared to healthy controls. No statistically significant differences were observed in the concentrations of the EV profiles among the DLBCL patients with and without VTE. Using Cox regression analysis, we found that none of the observed EV populations demonstrated an association with overall survival (OS). In conclusion, patients with DLBCL have elevated concentrations of distinct EV populations—in particular, PEVs, E-selectin EVs, P-selectin EVs, TF+/CD20+ EVs, and TF− DLBCL/B-cell EVs (CD19, CD20, CD45)—compared to healthy controls. DLBCL patients exhibit a specific EV profile, which is not significantly related to the risk of VTE and OS outcomes. Our data provide an intriguing insight into EV profiles in patients with DLBCL. Additional research is needed to elucidate these findings further. Full article

Review

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26 pages, 2209 KiB  
Review
Immunothrombosis in Sepsis: Cellular Crosstalk, Molecular Triggers, and Therapeutic Opportunities—A Review
by Addis Aklilu, Michael Siu-Lun Lai, Zhiwei Jiang, Shea Ping Yip and Chien-Ling Huang
Int. J. Mol. Sci. 2025, 26(13), 6114; https://doi.org/10.3390/ijms26136114 - 25 Jun 2025
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Abstract
Sepsis remains a critical global health challenge characterized by life-threatening organ dysfunction arising from a dysregulated host response to infection. Immunothrombosis refers to the intersection of immune activation and coagulation pathways, particularly relevant in the context of sepsis. A growing body of evidence [...] Read more.
Sepsis remains a critical global health challenge characterized by life-threatening organ dysfunction arising from a dysregulated host response to infection. Immunothrombosis refers to the intersection of immune activation and coagulation pathways, particularly relevant in the context of sepsis. A growing body of evidence identifies immunothrombosis, a tightly interwoven process between innate immunity and coagulation. While immunothrombosis serves as a host defense mechanism under physiological conditions, its aberrant activation in sepsis precipitates microvascular thrombosis, organ ischemia, and progression toward disseminated intravascular coagulation (DIC). This review provides a comprehensive overview of the cellular contributors to immunothrombosis, including neutrophils, monocytes, platelets, and endothelial cells, and elucidates the signaling cascades, such as nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and inflammasome activation, that govern their interplay. We further highlight emerging molecular mediators, including extracellular traps, tissue factor expression, and cytokine amplification loops, that collectively promote pathological thromboinflammation. A deeper understanding of these interconnected pathways offers critical insights into the pathogenesis of sepsis and unveils potential targets for timely intervention. Ultimately, this review aims to bridge immunological and hematological perspectives to inform the development of novel therapeutic strategies against sepsis-induced coagulopathy. Full article
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