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Biomolecules
Special Issues
Molecular Research on Thrombotic Microangiopathy and Thrombotic Complications
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Molecular Research on Thrombotic Microangiopathy and Thrombotic Complications

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

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 4004

Special Issue Editors

Dr. Pavel Avdonin

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Guest Editor
Koltzov Institute of Developmental Biology, Russian Academy of Sciences, RAS, Moscow, Russia
Interests: receptors; signalling systems; von Willebrand factor; endothelial cells; calcium; thrombotic microangiopathy
Dr. Galina A. Generalova

E-Mail Website
Guest Editor
Department of Pediatrics, Russian Medical Academy of Continuous Professional Education, Moscow, Russia
Interests: atypical HUS; complement; doppler ultrasonography; ultrasonography; diffusion magnetic resonance imaging
Dr. Vasily Nikolaevich Sukhorukov

E-Mail Website
Guest Editor
Petrovsky National Research Centre of Surgery, 2, Abrikosovsky Lane, 119991 Moscow, Russia
Interests: atherosclerosis; inflammation; macrophages; CRISPR/Cas9; low-density lipoprotein
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thrombotic microangiopathy (TMA) is a pathological syndrome characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and organ damage, primarily of the kidney and brain. Several approaches have been proposed for classification of TMA, each taking into account various aspects, such as genetic predisposition and secondary causes, violations of complement function or von Willebrand factor metabolism, dependence on pregnancy, transplantation, oncological diseases, the influence of drugs, etc. The molecular mechanisms causing TMA are diverse and not fully understood. The pathogenesis of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are the most studied forms of TMA. There is less clarity regarding other forms of TMA. The key reason for the development of TMA is damage of the microvascular endothelium. However, the mechanisms of endotheliopathy remain poorly understood. The purpose of this Special Issue is to present, analyze and summarize the latest data on the molecular and cellular mechanisms of the development of various forms of TMA and thrombotic complications. Of interest are articles that will characterize the pathogenetic mechanisms of TMA associated with other comorbidities. Another objective of the Issue is to consider the effectiveness of new approaches to the treatment of TMA, based on the use of new drugs that affect the main pathogenetic links of this disease.

Dr. Pavel Avdonin
Dr. Galina A. Generalova
Dr. Vasily Nikolaevich Sukhorukov
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • thrombotic mycroangiopathy
  • von Willebrand factor
  • endothelium
  • complement
  • hemolytic uremic syndrome
  • drugs
  • pathology
  • cardiovascular diseases
  • thrombotic complications
  • comorbidities

Published Papers (3 papers)

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Research

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15 pages, 2454 KiB  
Article
Effects of Antiplatelet Drugs on Platelet-Dependent Coagulation Reactions
by Ivan A. Muravlev, Anatoly B. Dobrovolsky, Olga A. Antonova, Svetlana G. Khaspekova, Amina K. Alieva, Dmitry V. Pevzner and Alexey V. Mazurov
Biomolecules 2023, 13(7), 1124; https://doi.org/10.3390/biom13071124 - 14 Jul 2023
Cited by 1 | Viewed by 1418
Abstract
Activated platelets are involved in blood coagulation by exposing phosphatidylserine (PS), which serves as a substrate for assembling coagulation complexes. Platelets accelerate fibrin formation and thrombin generation, two final reactions of the coagulation cascade. We investigated the effects of antiplatelet drugs on platelet [...] Read more.
Activated platelets are involved in blood coagulation by exposing phosphatidylserine (PS), which serves as a substrate for assembling coagulation complexes. Platelets accelerate fibrin formation and thrombin generation, two final reactions of the coagulation cascade. We investigated the effects of antiplatelet drugs on platelet impact in these reactions and platelet ability to expose PS. Washed human platelets were incubated with acetylsalicylic acid (ASA), ticagrelor, ASA in combination with ticagrelor, ruciromab (glycoprotein IIb-IIIa antagonist), or prostaglandin E1 (PGE1). Platelets were not activated or activated by collagen and sedimented in multiwell plates, and plasma was added after supernatant removal. Fibrin formation (clotting) was monitored in a recalcification assay by light absorbance and thrombin generation in a fluorogenic test. PS exposure was assessed by annexin V staining using flow cytometry. Ticagrelor (alone and in combination with ASA), ruciromab, and PGE1, but not ASA, prolonged the lag phase and decreased the maximum rate of plasma clotting and decreased the peak and maximum rate of thrombin generation. Inhibition was observed when platelets were not treated with exogenous agonists (activation by endogenous thrombin) and pretreated with collagen. Ticagrelor (alone and in combination with ASA), ruciromab, and PGE1, but not ASA, decreased PS exposure on washed platelets activated by thrombin and by thrombin + collagen. PS exposure on activated platelets in whole blood was lower in patients with acute coronary syndrome receiving ticagrelor + ASA in comparison with donors free of medications. These results indicate that antiplatelet drugs are able to suppress platelet coagulation activity not only in vitro but also after administration to patients. Full article
(This article belongs to the Special Issue Molecular Research on Thrombotic Microangiopathy and Thrombotic Complications)
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Review

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36 pages, 1895 KiB  
Review
The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome
by Piotr P. Avdonin, Maria S. Blinova, Galina A. Generalova, Khadizha M. Emirova and Pavel V. Avdonin
Biomolecules 2024, 14(1), 39; https://doi.org/10.3390/biom14010039 - 27 Dec 2023
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Abstract
Hemolytic uremic syndrome (HUS) is an acute disease and the most common cause of childhood acute renal failure. HUS is characterized by a triad of symptoms: microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. In most of the cases, HUS occurs as a [...] Read more.
Hemolytic uremic syndrome (HUS) is an acute disease and the most common cause of childhood acute renal failure. HUS is characterized by a triad of symptoms: microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. In most of the cases, HUS occurs as a result of infection caused by Shiga toxin-producing microbes: hemorrhagic Escherichia coli and Shigella dysenteriae type 1. They account for up to 90% of all cases of HUS. The remaining 10% of cases grouped under the general term atypical HUS represent a heterogeneous group of diseases with similar clinical signs. Emerging evidence suggests that in addition to E. coli and S. dysenteriae type 1, a variety of bacterial and viral infections can cause the development of HUS. In particular, infectious diseases act as the main cause of aHUS recurrence. The pathogenesis of most cases of atypical HUS is based on congenital or acquired defects of complement system. This review presents summarized data from recent studies, suggesting that complement dysregulation is a key pathogenetic factor in various types of infection-induced HUS. Separate links in the complement system are considered, the damage of which during bacterial and viral infections can lead to complement hyperactivation following by microvascular endothelial injury and development of acute renal failure. Full article
(This article belongs to the Special Issue Molecular Research on Thrombotic Microangiopathy and Thrombotic Complications)
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Other

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11 pages, 251 KiB  
Brief Report
A Moderate Decrease in ADAMTS13 Activity Correlates with the Severity of STEC-HUS
by Khadizha M. Emirova, Olga M. Orlova, Ekaterina M. Chichuga, Alexander L. Muzurov, Piotr P. Avdonin and Pavel V. Avdonin
Biomolecules 2023, 13(11), 1671; https://doi.org/10.3390/biom13111671 - 20 Nov 2023
Viewed by 920
Abstract
Atypical hemolytic uremic syndrome (HUS) develops as a result of damage to the endothelium of microvasculature vessels by Shiga toxin produced by enterohemorrhagic Escherichia coli (STEC-HUS). STEC-HUS remains the leading cause of acute kidney injury (AKI) in children aged 6 months to 5 [...] Read more.
Atypical hemolytic uremic syndrome (HUS) develops as a result of damage to the endothelium of microvasculature vessels by Shiga toxin produced by enterohemorrhagic Escherichia coli (STEC-HUS). STEC-HUS remains the leading cause of acute kidney injury (AKI) in children aged 6 months to 5 years. The pathomorphological essence of the disease is the development of thrombotic microangiopathy (TMA). One of the key causes of TMA is an imbalance in the ADAMTS13–von Willebrand factor (vWF)–platelet system. The goal of the work was to clarify the role of a moderate decrease in ADAMTS13 activity in the pathogenesis of STEC-HUS. The activity of ADAMTS13 was determined in 138 children (4 months–14.7 years) in the acute period of STEC-HUS and the features of the course of the disease in these patients were analyzed. The study revealed a decrease in the activity and concentration of ADAMTS13 in 79.8% and 90.6% of patients, respectively. Measurements of von Willebrand factor antigen content and the activity of von Willebrand factor in the blood plasma of part of these patients were carried out. In 48.6% and 34.4% of cases, there was an increase in the antigen concentration and the activity of the Willebrand factor, respectively. Thrombocytopenia was diagnosed in 97.8% of children. We have demonstrated that moderately reduced ADAMTS13 activity correlates with the risk of severe manifestations of STEC-HUS in children; the rate of developing multiple organ failure, cerebral disorders, pulmonary edema, and acute kidney injury with the need for dialysis increases. It is assumed that reduction in ADAMTS13 activity may serve as a predictor of disease severity. Full article
(This article belongs to the Special Issue Molecular Research on Thrombotic Microangiopathy and Thrombotic Complications)
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