Inflammation and Hemostasis: 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 953

Special Issue Editor


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Guest Editor
Division of Clinical Laboratory Science and Specialist Clinical Hemostasis Laboratory, Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary
Interests: hemostasis; thrombosis; fibrinolysis; factor XIII; stroke; cardiovascular diseases; clinical studies
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Special Issue Information

Dear Colleagues,

Inflammation and hemostasis are interrelated processes with extensive crosstalk affecting the balance of both systems. Although it was revealed more than 100 years ago that inflammation leads to excessive coagulation activation, more recently, the COVID-19 pandemic has again focused our attention on the importance of the link between these two systems. An excessive immune response may lead to a dysregulation of the hemostasis balance in numerous ways, which may result in thrombotic events, tissue damage, multiorgan failure, and death. Accumulating evidence suggests that the dysregulation of hemostasis, microvascular thrombosis, and hypercoagulability may not only occur during acute inflammatory events but may also play a significant role in the pathogenesis of a number of chronic inflammatory and autoimmune disorders. Although many aspects of the cellular and molecular interactions between hemostasis and inflammation have already been uncovered, today there is renewed interest in clarifying regulatory elements and undiscovered connections of the underlying pathways. Identifying molecular targets and triggers that are key players of the extensive crosstalk between coagulation and inflammation may provide promising therapeutic targets for both inflammatory and thrombotic disorders.

This Special Issue aims to focus on the complex interactions between inflammation and hemostasis, with special attention on the unique biological functions and molecular and cellular interactions between these pathways. Submission of original research articles and reviews is encouraged. Research areas may include (but are not limited to) the following:

  • Basic research studies exploring novel molecular or cellular interactions in the fields of inflammation and hemostasis (including animal models);
  • Clinical studies related to acute or chronic inflammatory states in patients and their effect on the hemostasis system (including studies on COVID-19);
  • Studies addressing novel therapeutic targets in inflammatory and/or hemostasis pathways;
  • Studies on novel methods, models, or biomarkers of related fields.

We look forward to receiving your contributions.

Dr. Zsuzsa Bagoly
Guest Editor

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Published Papers (1 paper)

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14 pages, 2903 KiB  
Article
Polysome Profiling Proves Impaired IL-10 and Caspase-8 Translation in PBMCs of Hemodialysis Patients
by Amanda Dawood, Roman Fiedler, Silke Markau, Matthias Girndt and Christof Ulrich
Biomolecules 2025, 15(3), 335; https://doi.org/10.3390/biom15030335 - 26 Feb 2025
Viewed by 390
Abstract
Triggered by uremic intoxication, a surplus of inflammatory mediators is present in the serum of hemodialysis (HD) patients. Anti-inflammatory counterbalancing mechanisms initiated by interleukin-10 (IL-10) and caspase-8 (Casp-8) appear to be disturbed. Earlier observations let us suppose that translational rather than transcriptional mechanisms [...] Read more.
Triggered by uremic intoxication, a surplus of inflammatory mediators is present in the serum of hemodialysis (HD) patients. Anti-inflammatory counterbalancing mechanisms initiated by interleukin-10 (IL-10) and caspase-8 (Casp-8) appear to be disturbed. Earlier observations let us suppose that translational rather than transcriptional mechanisms are responsible for this effect. Therefore, we investigated the polysome profiling of isolated PBMCs to study gene-specific mRNAs attached to monosomes and polysomes in HD patients (n = 42), patients with lipid disorder and normal renal function (LD, n = 10) and healthy control subjects (CO, n = 9). CRP (C-reactive protein) as a marker of inflammation was significantly elevated in HD and LD patients compared to CO subjects. NGAL (neutrophil-associated lipocalin), a potential marker of kidney disease and inflammation was increased in HD versus LD and CO. LD patients, however, had significantly higher proteosomal IL-10 and Casp-8 activities. LD and HD are two high cardiovascular risk groups with microinflammation. Lower translational activities of IL-10 and Casp-8 mRNAs in HD may be the result of a weak anti-inflammatory response potentially associated with the uremic immune defect. Full article
(This article belongs to the Special Issue Inflammation and Hemostasis: 2nd Edition)
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