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Special Issue "Platelet Signaling and Coagulation"

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 (31 August 2023) | Viewed by 989

Special Issue Editors

College of Pharmacy and Health Sciences, Campbell University, Buies Creek, NC 27506, USA
Interests: platelets; ether lipids; hemostasis; signaling; thrombosis
LSU Health Science Center, New Orleans, LA 70112, USA
Interests: coagulation; anticoagulants; platelets; haemostasis; thrombosis; procoagulants; hypoxia

Special Issue Information

Dear Colleagues,

Circulating platelets are highly reactive cell types that respond to a myriad of environmental cues to form homotypic aggregates as well as heterotypic interactions with leukocytes and endothelia. These events not only support a spectrum of normal homeostatic processes such as blood vessel integrity, initiation of the coagulation cascade, and immunological responses, but also ischemic pathologies and coagulopathies. Signaling events within platelets are well understood, but new inputs and modulators are being identified that provide insight as to how platelets produce unique responses in vivo.

This Special Issue of the International Journal of Molecular Sciences, entitled “Platelet Signaling and Coagulation”, will emphasize signaling pathways leading to critical platelet functions in hemostasis, coagulopathy, and thrombosis. The goal is to provide a broad view of platelet reactivity at the molecular level in a variety of physiological contexts. We invite you to contribute original research or focused reviews on the above topics for this Special Issue. We particularly welcome submissions from postdocs, PhD students, and young researchers.

We look forward to reading about your insights and exciting discoveries that further advance our knowledge of this crucial cell type in health and disease.

Dr. Stephen P. Holly
Dr. Rinku Majumder
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.


  • platelet
  • signaling
  • coagulation
  • aggregation
  • thrombosis
  • hemostasis
  • protein S
  • COVID-19

Published Papers (1 paper)

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Systemic Review of Clot Retraction Modulators
Int. J. Mol. Sci. 2023, 24(13), 10602; https://doi.org/10.3390/ijms241310602 - 25 Jun 2023
Viewed by 702
Through a process termed clot retraction, platelets cause thrombi to shrink and become more stable. After platelets are activated via inside-out signaling, glycoprotein αIIbβIII binds to fibrinogen and initiates a cascade of intracellular signaling that ends in actin remodeling, which causes the [...] Read more.
Through a process termed clot retraction, platelets cause thrombi to shrink and become more stable. After platelets are activated via inside-out signaling, glycoprotein αIIbβIII binds to fibrinogen and initiates a cascade of intracellular signaling that ends in actin remodeling, which causes the platelet to change its shape. Clot retraction is also important for wound healing. Although the detailed molecular biology of clot retraction is only partially understood, various substances and physiological conditions modulate clot retraction. In this review, we describe some of the current literature pertaining to clot retraction modulators. In addition, we discuss compounds from Cudrania trucuspidata, Arctium lappa, and Panax ginseng that diminish clot retraction and have numerous other health benefits. Caffeic acid and diindolylmethane, both common in plants and vegetables, likewise reduce clot retraction, as do all-trans retinoic acid (a vitamin A derivative), two MAP4K inhibitors, and the chemotherapeutic drug Dasatinib. Conversely, the endogenous anticoagulant Protein S (PS) and the matricellular protein secreted modular calcium-binding protein 1 (SMOC1) both enhance clot retraction. Most studies aiming to identify mechanisms of clot retraction modulators have focused on the increased phosphorylation of vasodilator-stimulated phosphoprotein and inositol 1,4,5-triphosphate receptor I and the decreased phosphorylation of various phospholipases (e.g., phospholipase A2 (PLA2) and phosphatidylinositol-specific phospholipase Cγ2 (PLCγ2), c-Jun N-terminal kinase, and (PI3Ks). One study focused on the decreased phosphorylation of Sarcoma Family Kinases (SFK), and others have focused on increased cAMP levels and the downregulation of inflammatory markers such as thromboxanes, including thromboxane A2 (TXA2) and thromboxane B2 (TXB2); prostaglandin A2 (PGE2); reactive oxygen species (ROS); and cyclooxygenase (COX) enzyme activity. Additionally, pregnancy, fibrinolysis, and the autoimmune condition systemic lupus erythematosus all seem to affect, or at least have some relation with, clot retraction. All the clot retraction modulators need in-depth study to explain these effects. Full article
(This article belongs to the Special Issue Platelet Signaling and Coagulation)
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