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Special Issue "Molecular Pathways for Vascular Risk in Diabetes"

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

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editor

Prof. Dr. Ramzi Ajjan
E-Mail Website
Guest Editor
Leeds Institute for Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK
Interests: glycaemia in diabetes; thrombosis in diabetes; reduction of cardiovascular risk in diabetes

Special Issue Information

Dear Colleagues,

Cardiovascular disease remains the main cause of morbidity and mortality in patients with diabetes. It is now generally acknowledged that diabetes is a continuum of various stages of the condition, with each having a different vascular risk. The reasons for the adverse vascular profile in diabetes are related to a combination of more extensive atherosclerotic disease coupled with an enhanced thrombotic environment.

This Special Issue is particularly interested in collecting research articles, comprehensive reviews, or short communications in the following topics, but all other related topics are welcomed.

  1. Molecular mechanisms linking complements proteins with increased thrombosis risk, particularly in diabetes;
  2. Hypoglycemia, glycemic variability, and vascular pathology in diabetes;
  3. Novel insights into platelet function/dysfunction in diabetes: Implications for future anti-thrombotic therapies;
  4. Inflammation and atherothrombosis: relevance in diabetes;
  5. Molecular mechanisms for the vascular and cardiac benefits of sodium glucose transporter-2 inhibitors (SGLT2).

Prof. Dr. Ramzi Ajjan
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 papers will be 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.

Published Papers (2 papers)

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Review

Review
Glucose Variability: How Does It Work?
Int. J. Mol. Sci. 2021, 22(15), 7783; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22157783 - 21 Jul 2021
Viewed by 563
Abstract
A growing body of evidence points to the role of glucose variability (GV) in the development of the microvascular and macrovascular complications of diabetes. In this review, we summarize data on GV-induced biochemical, cellular and molecular events involved in the pathogenesis of diabetic [...] Read more.
A growing body of evidence points to the role of glucose variability (GV) in the development of the microvascular and macrovascular complications of diabetes. In this review, we summarize data on GV-induced biochemical, cellular and molecular events involved in the pathogenesis of diabetic complications. Current data indicate that the deteriorating effect of GV on target organs can be realized through oxidative stress, glycation, chronic low-grade inflammation, endothelial dysfunction, platelet activation, impaired angiogenesis and renal fibrosis. The effects of GV on oxidative stress, inflammation, endothelial dysfunction and hypercoagulability could be aggravated by hypoglycemia, associated with high GV. Oscillating hyperglycemia contributes to beta cell dysfunction, which leads to a further increase in GV and completes the vicious circle. In cells, the GV-induced cytotoxic effect includes mitochondrial dysfunction, endoplasmic reticulum stress and disturbances in autophagic flux, which are accompanied by reduced viability, activation of apoptosis and abnormalities in cell proliferation. These effects are realized through the up- and down-regulation of a large number of genes and the activity of signaling pathways such as PI3K/Akt, NF-κB, MAPK (ERK), JNK and TGF-β/Smad. Epigenetic modifications mediate the postponed effects of glucose fluctuations. The multiple deteriorative effects of GV provide further support for considering it as a therapeutic target in diabetes. Full article
(This article belongs to the Special Issue Molecular Pathways for Vascular Risk in Diabetes)
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Review
PAI-1 in Diabetes: Pathophysiology and Role as a Therapeutic Target
Int. J. Mol. Sci. 2021, 22(6), 3170; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063170 - 20 Mar 2021
Cited by 2 | Viewed by 658
Abstract
Hypofibrinolysis is a key abnormality in diabetes and contributes to the adverse vascular outcome in this population. Plasminogen activator inhibitor (PAI)-1 is an important regulator of the fibrinolytic process and levels of this antifibrinolytic protein are elevated in diabetes and insulin resistant states. [...] Read more.
Hypofibrinolysis is a key abnormality in diabetes and contributes to the adverse vascular outcome in this population. Plasminogen activator inhibitor (PAI)-1 is an important regulator of the fibrinolytic process and levels of this antifibrinolytic protein are elevated in diabetes and insulin resistant states. This review describes both the physiological and pathological role of PAI-1 in health and disease, focusing on the mechanism of action as well as protein abnormalities in vascular disease with special focus on diabetes. Attempts at inhibiting protein function, using different techniques, are also discussed including direct and indirect interference with production as well as inhibition of protein function. Developing PAI-1 inhibitors represents an alternative approach to managing hypofibrinolysis by targeting the pathological abnormality rather than current practice that relies on profound inhibition of the cellular and/or acellular arms of coagulation, and which can be associated with increased bleeding events. The review offers up-to-date knowledge on the mechanisms of action of PAI-1 together with the role of altering protein function to improve hypofirbinolysis. Developing PAI-1 inhibitors may form for the basis of future new class of antithrombotic agents that reduce vascular complications in diabetes. Full article
(This article belongs to the Special Issue Molecular Pathways for Vascular Risk in Diabetes)
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