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Genetic, Functional and Therapeutic Aspects of Procoagulant and Anticoagulant Factors 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 3500

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Special Issue Editors

Prof. Tami Livnat

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Guest Editor

1. Director, Amalia Biron Research Institute of Thrombosis and Hemostasis, Faculty of Medical and Health Sciences, Tel-Aviv University Sheba Medical Center, Tel Hashomer 52621, Israel
2. Rabin Medical Centre, Ophthalmology Department and Laboratory of Eye Research Felsenstein Medical Research Centre, Petah-Tikva 49100, Israel
Interests: procoagulant factors; anticoagulant factors; hemostasis; neuroprotection; ocular diseases
Special Issues, Collections and Topics in MDPI journals

Dr. Rima Dardik

E-Mail Website
Guest Editor

National Hemophilia Center, Sheba Medical Center, Ramat Gan 52621, Israel
Interests: procoagulant factors; anticoagulant factors; hemostasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Normal hemostasis is highly dependent on the balance between procoagulant systems (e.g., platelets and procoagulant factors) and anticoagulant systems (e.g., protein C, protein S and antithrombin). The lack or dysfunction of a major procoagulant factor results in a bleeding disorder (e.g., factor VIII deficiency leading to hemophilia A), whereas a defect in an essential anticoagulant system (e.g. protein C deficiency) leads to a thrombotic disorder. Beyond their function in hemostasis, cell signaling pathways that are induced by procoagulant (e.g., thrombin and FVII) and anticoagulant factors (e.g., APC), mediated by specific receptors, have become the focus of increasing attention, with some of them being explored as promising therapeutic targets.

This Special Issue will focus on the genetic, functional and therapeutic aspects of procoagulant and anticoagulant systems. We invite research studies and reviews on the genetics of bleeding and thrombotic disorders annd functional and therapeutic studies of procoagulant and anticoagulant factors, as well as studies that explore their involvement in the crosstalk between hemostasis and inflammation.

Prof. Tami Livnat
Dr. Rima Dardik
Guest Editors

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

procoagulant factors
anticoagulant factors
hemostasis
inflammation
genetics
therapeutics
cell signaling

Published Papers (3 papers)

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Research

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14 pages, 758 KiB

Open AccessArticle

Association of Thymidylate Synthase (TS) Gene Polymorphisms with Incidence and Prognosis of Coronary Artery Disease

by Jung Oh Kim, Chang Soo Ryu, Jeong Yong Lee, Eun Ju Ko, Yong Hyun Ha, Jung Hoon Sung, Tae Sun Hwang, In Jai Kim and Nam Keun Kim

Int. J. Mol. Sci. 2023, 24(16), 12591; https://doi.org/10.3390/ijms241612591 - 09 Aug 2023

Cited by 1 | Viewed by 773

Abstract

Coronary artery disease (CAD) is a prevalent cardiovascular condition characterized by the accumulation of plaque within coronary arteries. While distinct features of CAD have been reported, the association between genetic factors and CAD in terms of biomarkers was insufficient. This study aimed to investigate the connection between genetic factors and CAD, focusing on the thymidylate synthase (TS) gene, a gene involved in DNA synthesis and one-carbon metabolism. TS plays a critical role in maintaining the deoxythymidine monophosphate (dTMP) pool, which is essential for DNA replication and repair. Therefore, our research targeted single nucleotide polymorphisms that could potentially impact TS gene expression and lead to dysfunction. Our findings strongly associate the TS 1100T>C and 1170A>G genotypes with CAD susceptibility. We observed that TS 1100T>C polymorphisms increased disease susceptibility in several groups, while the TS 1170A>G polymorphism displayed a decreasing trend for disease risk when interacting with clinical factors. Furthermore, our results demonstrate the potential contribution of the TS 1100/1170 haplotypes to disease susceptibility, indicating a synergistic interaction with clinical factors in disease occurrence. Based on these findings, we propose that polymorphisms in the TS gene had the possibility of clinically useful biomarkers for the prevention, prognosis, and management of CAD in the Korean population. Full article

(This article belongs to the Special Issue Genetic, Functional and Therapeutic Aspects of Procoagulant and Anticoagulant Factors 2.0)

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17 pages, 19070 KiB

Open AccessArticle

3K3A-Activated Protein C Inhibits Choroidal Neovascularization Growth and Leakage and Reduces NLRP3 Inflammasome, IL-1β, and Inflammatory Cell Accumulation in the Retina

by Yehonatan Weinberger, Ivan Budnik, Yael Nisgav, Dahlia Palevski, Gil Ben-David, José A. Fernández, Shany Nivinsky Margalit, Sarina Levy-Mendelovich, Gili Kenet, Dov Weinberger, John H. Griffin and Tami Livnat

Int. J. Mol. Sci. 2023, 24(13), 10642; https://doi.org/10.3390/ijms241310642 - 26 Jun 2023

Viewed by 1100

Abstract

3K3A-Activated Protein C (APC) is a recombinant variant of the physiological anticoagulant APC with cytoprotective properties and reduced bleeding risks. We studied the potential use of 3K3A-APC as a multi-target therapeutic option for choroidal neovascularization (CNV), a common cause of vision loss in age-related macular degeneration. CNV was induced by laser photocoagulation in a murine model, and 3K3A-APC was intravitreally injected. The impact of 3K3A-APC treatment on myeloid and microglia cell activation and recruitment and on NLRP3 inflammasome, IL-1β, and VEGF levels was assessed using cryosection, retinal flat-mount immunohistochemistry and vascular imaging. Additionally, we evaluated the use of fluorescein angiography as a surrogate marker for in vivo evaluation of the efficacy of 3K3A-APC treatment against leaking CNV lesions. Our results demonstrated that 3K3A-APC treatment significantly reduced the accumulation and activation of myeloid cells and microglia in the CNV area and decreased the NLRP3 and IL-1β levels at the CNV site and the surrounding retina. Furthermore, 3K3A-APC treatment resulted in leakage regression and CNV growth suppression. These findings indicate that the anti-inflammatory activities of 3K3A-APC contribute to CNV inhibition. Our study suggests the potential use of 3K3A-APC as a novel multi-target treatment for CNV. Full article

(This article belongs to the Special Issue Genetic, Functional and Therapeutic Aspects of Procoagulant and Anticoagulant Factors 2.0)

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Review

Jump to: Research

20 pages, 4013 KiB

Open AccessReview

Could Cyclosiversioside F Serve as a Dietary Supplement to Prevent Obesity and Relevant Disorders?

by Siqi Qin, Junren Chen, Kexin Zhong, Dan Li and Cheng Peng

Int. J. Mol. Sci. 2023, 24(18), 13762; https://doi.org/10.3390/ijms241813762 - 06 Sep 2023

Cited by 2 | Viewed by 1164

Abstract

Obesity is the basis of numerous metabolic diseases and has become a major public health issue due to its rapidly increasing prevalence. Nevertheless, current obesity therapeutic strategies are not sufficiently effective, so there is an urgent need to develop novel anti-obesity agents. Naturally occurring saponins with outstanding bio-activities have been considered promising drug leads and templates for human diseases. Cyclosiversioside F (CSF) is a paramount multi-functional saponin separated from the roots of the food-medicinal herb Astragali Radix, which possesses a broad spectrum of bioactivities, including lowering blood lipid and glucose, alleviating insulin resistance, relieving adipocytes inflammation, and anti-apoptosis. Recently, the therapeutic potential of CSF in obesity and relevant disorders has been gradually explored and has become a hot research topic. This review highlights the role of CSF in treating obesity and obesity-induced complications, such as diabetes mellitus, diabetic nephropathy, cardiovascular and cerebrovascular diseases, and non-alcoholic fatty liver disease. Remarkably, the underlying molecular mechanisms associated with CSF in disease therapy have been partially elucidated, especially PI3K/Akt, NF-κB, MAPK, apoptotic pathway, TGF-β, NLRP3, Nrf-2, and AMPK, with the aim of promoting the development of CSF as a functional food and providing references for its clinical application in obesity-related disorders therapy. Full article

(This article belongs to the Special Issue Genetic, Functional and Therapeutic Aspects of Procoagulant and Anticoagulant Factors 2.0)

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