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Advances in Biological Function of Fibrinogen and Fibrin

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

Deadline for manuscript submissions: closed (30 April 2020) | Viewed by 30765

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Special Issue Editor

Dr. Abha Sahni

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Guest Editor

Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, TX, USA
Interests: intracellular bacteria; endothelium; infection; pathogenesis; host-pathogen interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since its discovery over three centuries ago, studies on fibrinogen and fibrin (fibrin(ogen)) have led to remarkable advances in structure–function analysis, as well as evidence for the involvement of this versatile biological molecule in multiple physiological and pathological scenarios, including cardiovascular ailments, inflammation, infection, tumour growth and metastasis, and neurological disorders. Interactions of fibrin(ogen) with plasma proteins and receptors on the platelets, leukocytes, endothelial cells, and other cells, regulate a multitude of signalling pathways as well as their downstream consequences. Alterations in the levels and/or functions of fibrin(ogen) increase the risk of haemorrhage, thrombosis, infection, inflammation, and many other disease states. Genetic and pharmacologic approaches have further ascertained the important contributions of fibrinogen during local or systemic inflammation. A collection of cellular and molecular analyses further project fibrin(ogen) as a signalling molecule, determining the balance between haemostasis and thrombosis, coagulation and fibrosis, and eventually life and death. Continued efforts to enhance our understanding of the roles of fibrinogen and fibrin in these processes are likely to advance treatment options and the prevention of many human diseases.

This Special Issue on “Advances in Biological Functions of Fibrinogen and Fibrin” invites original research, reviews, and perspectives focused on all aspects of fibrinogen and fibrin, and aims to provide a comprehensive summary of the ongoing biomedical research on the roles of fibrin(ogen) in thrombosis, haemostasis, and other diseases.

Prof. Dr. Abha Sahni
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Fibrinogen
Fibrin
Thrombosis
Cancer
Metastasis
Infection
Inflammation
Cardiovascular
Signaling

Published Papers (3 papers)

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Research

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14 pages, 1466 KiB

Open AccessArticle

by Ryuta Nakae, Yu Fujiki, Yasuhiro Takayama, Takahiro Kanaya, Yutaka Igarashi, Go Suzuki, Yasutaka Naoe and Shoji Yokobori

Int. J. Mol. Sci. 2020, 21(16), 5613; https://doi.org/10.3390/ijms21165613 - 5 Aug 2020

Cited by 12 | Viewed by 3149

Abstract

Coagulopathy and older age are common and well-recognized risk factors for poorer outcomes in traumatic brain injury (TBI) patients; however, the relationships between coagulopathy and age remain unclear. We hypothesized that coagulation/fibrinolytic abnormalities are more pronounced in older patients and may be a factor in poorer outcomes. We retrospectively evaluated severe TBI cases in which fibrinogen and D-dimer were measured on arrival and 3–6 h after injury. Propensity score-matched analyses were performed to adjust baseline characteristics between older patients (the “elderly group,” aged ≥75 y) and younger patients (the “non-elderly group,” aged 16–74 y). A total of 1294 cases (elderly group: 395, non-elderly group: 899) were assessed, and propensity score matching created a matched cohort of 324 pairs. Fibrinogen on admission, the degree of reduction in fibrinogen between admission and 3–6 h post-injury, and D-dimer levels between admission and 3–6 h post-injury were significantly more abnormal in the elderly group than in the non-elderly group. On multivariate logistic regression analysis, independent risk factors for poor prognosis included low fibrinogen and high D-dimer levels on admission. Posttraumatic coagulation and fibrinolytic abnormalities are more severe in older patients, and fibrinogen and D-dimer abnormalities are negative predictive factors. Full article

(This article belongs to the Special Issue Advances in Biological Function of Fibrinogen and Fibrin)

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Review

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25 pages, 9083 KiB

Open AccessReview

Covid-19: The Rollercoaster of Fibrin(Ogen), D-Dimer, Von Willebrand Factor, P-Selectin and Their Interactions with Endothelial Cells, Platelets and Erythrocytes

by Corlia Grobler, Siphosethu C. Maphumulo, L. Mireille Grobbelaar, Jhade C. Bredenkamp, Gert J. Laubscher, Petrus J. Lourens, Janami Steenkamp, Douglas B. Kell and Etheresia Pretorius

Int. J. Mol. Sci. 2020, 21(14), 5168; https://doi.org/10.3390/ijms21145168 - 21 Jul 2020

Cited by 119 | Viewed by 20070

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2), also known as coronavirus disease 2019 (COVID-19)-induced infection, is strongly associated with various coagulopathies that may result in either bleeding and thrombocytopenia or hypercoagulation and thrombosis. Thrombotic and bleeding or thrombotic pathologies are significant accompaniments to acute respiratory syndrome and lung complications in COVID-19. Thrombotic events and bleeding often occur in subjects with weak constitutions, multiple risk factors and comorbidities. Of particular interest are the various circulating inflammatory coagulation biomarkers involved directly in clotting, with specific focus on fibrin(ogen), D-dimer, P-selectin and von Willebrand Factor (VWF). Central to the activity of these biomarkers are their receptors and signalling pathways on endothelial cells, platelets and erythrocytes. In this review, we discuss vascular implications of COVID-19 and relate this to circulating biomarker, endothelial, erythrocyte and platelet dysfunction. During the progression of the disease, these markers may either be within healthy levels, upregulated or eventually depleted. Most significant is that patients need to be treated early in the disease progression, when high levels of VWF, P-selectin and fibrinogen are present, with normal or slightly increased levels of D-dimer (however, D-dimer levels will rapidly increase as the disease progresses). Progression to VWF and fibrinogen depletion with high D-dimer levels and even higher P-selectin levels, followed by the cytokine storm, will be indicative of a poor prognosis. We conclude by looking at point-of-care devices and methodologies in COVID-19 management and suggest that a personalized medicine approach should be considered in the treatment of patients. Full article

(This article belongs to the Special Issue Advances in Biological Function of Fibrinogen and Fibrin)

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19 pages, 2190 KiB

Open AccessReview

Genetic Variants in the FGB and FGG Genes Mapping in the Beta and Gamma Nodules of the Fibrinogen Molecule in Congenital Quantitative Fibrinogen Disorders Associated with a Thrombotic Phenotype

by Tomas Simurda, Monika Brunclikova, Rosanna Asselta, Sonia Caccia, Jana Zolkova, Zuzana Kolkova, Dusan Loderer, Ingrid Skornova, Jan Hudecek, Zora Lasabova, Jan Stasko and Peter Kubisz

Int. J. Mol. Sci. 2020, 21(13), 4616; https://doi.org/10.3390/ijms21134616 - 29 Jun 2020

Cited by 38 | Viewed by 4834

Abstract

Fibrinogen is a hexameric plasmatic glycoprotein composed of pairs of three chains (Aα, Bβ, and γ), which play an essential role in hemostasis. Conversion of fibrinogen to insoluble polymer fibrin gives structural stability, strength, and adhesive surfaces for growing blood clots. Equally important, the exposure of its non-substrate thrombin-binding sites after fibrin clot formation promotes antithrombotic properties. Fibrinogen and fibrin have a major role in multiple biological processes in addition to hemostasis and thrombosis, i.e., fibrinolysis (during which the fibrin clot is broken down), matrix physiology (by interacting with factor XIII, plasminogen, vitronectin, and fibronectin), wound healing, inflammation, infection, cell interaction, angiogenesis, tumour growth, and metastasis. Congenital fibrinogen deficiencies are rare bleeding disorders, characterized by extensive genetic heterogeneity in all the three genes: FGA, FGB, and FGG (enconding the Aα, Bβ, and γ chain, respectively). Depending on the type and site of mutations, congenital defects of fibrinogen can result in variable clinical manifestations, which range from asymptomatic conditions to the life-threatening bleeds or even thromboembolic events. In this manuscript, we will briefly review the main pathogenic mechanisms and risk factors leading to thrombosis, and we will specifically focus on molecular mechanisms associated with mutations in the C-terminal end of the beta and gamma chains, which are often responsible for cases of congenital afibrinogenemia and hypofibrinogenemia associated with thrombotic manifestations. Full article

(This article belongs to the Special Issue Advances in Biological Function of Fibrinogen and Fibrin)

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