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Medicina
Special Issues
Endotheliopathy: Its Pathogenesis and Dysfunction Syndromes
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Endotheliopathy: Its Pathogenesis and Dysfunction Syndromes

A special issue of Medicina (ISSN 1648-9144).

Deadline for manuscript submissions: closed (15 May 2022) | Viewed by 3674

Special Issue Editors

Dr. Vijay Avin

E-Mail Website
Guest Editor
Department of Pharmacology and Regenerative Medicine, University of Illinois at Chicago, Chicago, IL, USA
Interests: vascular biology; endothelial cell signalling; tumor angiogenesis
Special Issues, Collections and Topics in MDPI journals
Dr. Deborah Fratantonio

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnology and Biopharmaceutics, University of Bari Aldo Moro, 70125 Bari, Italy
Interests: extracellular vesicles; endothelial dysfunction; mitochondrial homeostasis

Special Issue Information

Dear Colleagues, 

The vascular endothelium forms the innermost layer of all blood vessels and has the vital task of providing nutrients to the underlying tissue while limiting the access of macromolecules and leukocytes. Loss of endothelial barrier function leads to life-threatening inflammatory diseases such as acute lung injury (ALI), deregulated angiogenesis, tumor angiogenesis, and vascular-associated diabetic retinopathy. Over time, the standard therapeutics of diseases caused due to endothelial cell (EC) dysfunction has evolved, which however has further the scope due to the conundrum of their off-target/on-target effects. There is an unmet need to understand the cellular and molecular aspects of EC-dysfunction-associated diseases that form the basis of their correct clinical understanding and pathology-based diagnostics. This Special Issue entitled “Endotheliopathy: Its Pathogenesis and Dysfunction Syndromes” focuses on EC injury and dysfunction with the aim of presenting an update of current understanding as well as the development of therapeutics and their implications. This will cover original/review/clinical/translational study papers related to the molecular mechanism of endothelial-dysfunction-associated diseases, diagnosis, and treatment.

Dr. Vijay Avin
Dr. Deborah Fratantonio
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. Medicina 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 1800 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

  • endothelial cells
  • angiogenesis
  • tumor-associated endothelial cells
  • endothelial barrier dysfunction
  • endothelial cell transition
  • endothelial progenitor cells
  • endothelial cell-targeted therapy
  • pulmonary vascular injury
  • brain vasculature

Published Papers (1 paper)

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Review

28 pages, 1668 KiB  
Review
Molecular Pathogenesis of Endotheliopathy and Endotheliopathic Syndromes, Leading to Inflammation and Microthrombosis, and Various Hemostatic Clinical Phenotypes Based on “Two-Activation Theory of the Endothelium” and “Two-Path Unifying Theory” of Hemostasis
by Jae C. Chang
Medicina 2022, 58(9), 1311; https://doi.org/10.3390/medicina58091311 - 19 Sep 2022
Cited by 6 | Viewed by 2904
Abstract
Endotheliopathy, according to the “two-activation theory of the endothelium”, can be triggered by the activated complement system in critical illnesses, such as sepsis and polytrauma, leading to two distinctly different molecular dysfunctions: (1) the activation of the inflammatory pathway due to the release [...] Read more.
Endotheliopathy, according to the “two-activation theory of the endothelium”, can be triggered by the activated complement system in critical illnesses, such as sepsis and polytrauma, leading to two distinctly different molecular dysfunctions: (1) the activation of the inflammatory pathway due to the release of inflammatory cytokines, such as interleukin 6 and tumor necrosis factor-α, and (2) the activation of the microthrombotic pathway due to the exocytosis of hemostatic factors, such as ultra-large von Willebrand factor (ULVWF) multimers and FVIII. The former promotes inflammation, including inflammatory organ syndrome (e.g., myocarditis and encephalitis) and multisystem inflammatory syndrome (e.g., cytokine storm), and the latter provokes endotheliopathy-associated vascular microthrombotic disease (VMTD), orchestrating thrombotic thrombocytopenic purpura (TTP)-like syndrome in arterial endotheliopathy, and immune thrombocytopenic purpura (ITP)-like syndrome in venous endotheliopathy, as well as multiorgan dysfunction syndrome (MODS). Because the endothelium is widely distributed in the entire vascular system, the phenotype manifestations of endotheliopathy are variable depending on the extent and location of the endothelial injury, the cause of the underlying pathology, as well as the genetic factor of the individual. To date, because the terms of many human diseases have been defined based on pathological changes in the organ and/or physiological dysfunction, endotheliopathy has not been denoted as a disease entity. In addition to inflammation, endotheliopathy is characterized by the increased activity of FVIII, overexpressed ULVWF/VWF antigen, and insufficient ADAMTS13 activity, which activates the ULVWF path of hemostasis, leading to consumptive thrombocytopenia and microthrombosis. Endothelial molecular pathogenesis produces the complex syndromes of inflammation, VMTD, and autoimmunity, provoking various endotheliopathic syndromes. The novel conceptual discovery of in vivo hemostasis has opened the door to the understanding of the pathogeneses of many endotheliopathy-associated human diseases. Reviewed are the hemostatic mechanisms, pathogenesis, and diagnostic criteria of endotheliopathy, and identified are some of the endotheliopathic syndromes that are encountered in clinical medicine. Full article
(This article belongs to the Special Issue Endotheliopathy: Its Pathogenesis and Dysfunction Syndromes)
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