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Special Issue "Molecular Advances in Hypertension and Blood"

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: closed (28 March 2021) | Viewed by 5363

Special Issue Editors

Dr. Eleni Gavriilaki
E-Mail Website
Guest Editor
Hematology Department, Bone Marrow Transplantation Unit, G. Papanicolaou Hospital, 57010 Thessaloniki, Greece
Interests: thrombotic microangiopathy; complement; complement inhibitors; hematopoietic cell transplantation; atypical hemolytic uremic syndrome; COVID-19; thrombotic thrombocytopenic purpura
Special Issues, Collections and Topics in MDPI journals
Dr. Eugenia Gkaliagkousi
E-Mail
Guest Editor
Aristotle University of Thessaloniki, Thessaloniki, Greece
Interests: arterial hypertension; endothelial dysfunction; platelets; arterial stiffness; microvesicles; dipping; nitric oxide; cardiovascular risk

Special Issue Information

Dear Colleagues,

We are launching a Special Issue on “Molecular Advances in Hypertension and Blood”. Our Special Issue will address the topic from both sides of the coin.

Firstly, we plan to investigate the interesting and under-reported pathophysiology of hypertension in hematological oncology and hematopoietic cell transplantation. Although neglected, hypertension is not only a key diagnostic and prognostic clinical finding in acute syndromes, such as thrombotic microangiopathy, but also a late effect of long-term survivors leading to increased cardiovascular and cerebrovascular mortality. This Special Issue will cover molecular advances in this field, exploring the role of genetics and epigenetics components, the renin–angiotensin aldosterone system, the autonomous nervous system, as well as the role of the aging vascular tree and endothelium.

Secondly, hematopoietic cells and their microvesicles have recently emerged as novel markers of cardiovascular risk. The crosstalk between these vesicles and endothelial dysfunction or vascular damage is a field of continuous progress. Apart from being biomarkers, these could also pose promising therapeutic targets in the future. Thromboinflammation represents an emerging concept in cardiovascular diseases. Novel insights into the role of hematopoietic cells in hypertension will be covered in this Special Issue.

Realizing the unmet needs of increased awareness of treating physicians and active researchers in this complex setting, we propose this Special Issue. Since IJMS is a journal of molecular science, we will accept translational studies with biomolecular experiments. We hope that you will find it of interest and submit your valuable research.

Dr. Eleni Gavriilaki
Dr. Eugenia Gkaliagkousi
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

  • arterial hypertension
  • microvesicles
  • endothelial dysfunction
  • platelets
  • thrombotic microangiopathy
  • complement
  • hematopoietic cell transplantation
  • cardiovascular risk

Published Papers (5 papers)

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Editorial

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Editorial
Molecular Advances in Hypertension and Blood
Int. J. Mol. Sci. 2022, 23(1), 278; https://doi.org/10.3390/ijms23010278 - 28 Dec 2021
Viewed by 518
Abstract
Hematopoietic cells and their microvesicles have recently emerged as novel markers of cardiovascular risk [...] Full article
(This article belongs to the Special Issue Molecular Advances in Hypertension and Blood)

Research

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Article
Myocardial Hypertrophy and Fibrosis Are Associated with Cardiomyocyte Beta-Catenin and TRPC6/Calcineurin/NFAT Signaling in Spontaneously Hypertensive Rats with 5/6 Nephrectomy
Int. J. Mol. Sci. 2021, 22(9), 4645; https://doi.org/10.3390/ijms22094645 - 28 Apr 2021
Cited by 2 | Viewed by 1042
Abstract
Background: Arterial hypertension (AH) is associated with heart and chronic kidney disease (CKD). However, the precise mechanisms of myocardial remodeling (MR) in the settings of CKD remain elusive. We hypothesized that TRPC6, calcineurin/NFAT, and Wnt/β-catenin signaling pathways are involved in the development of [...] Read more.
Background: Arterial hypertension (AH) is associated with heart and chronic kidney disease (CKD). However, the precise mechanisms of myocardial remodeling (MR) in the settings of CKD remain elusive. We hypothesized that TRPC6, calcineurin/NFAT, and Wnt/β-catenin signaling pathways are involved in the development of MR in the background of CKD and AH. Methods: Early CKD was induced by performing a 5/6 nephrectomy (5/6NE) in spontaneously hypertensive rats (SHR-NE). Sham-operated (SO) SHR (SHR-SO) and Wistar Kyoto (WKY-SO) rats served as controls. Systolic blood pressure (SBP), heart rate, myocardial mass index (MMI), serum creatinine, cardiomyocyte diameter (dCM), myocardial fibrosis (MF), serum and kidney α-Klotho levels, myocardial expression of calcineurin (CaN), TRPC6, and β-catenin were measured two months after 5/6NE or SO. Results: NE-induced kidney dysfunction corresponded to mild-to-moderate human CKD and was associated with an increase in FGF23 and a decrease in renal α-Klotho. The levels of SBP, MMI, dCM, and MF were higher in SHRs compared to WKY-SO as well as in SHR-NE vs. SHR-SO. The MR was associated with increased cardiomyocyte expression of CaN/NFAT and β-catenin along with its intracellular re-distribution. TRPC6 protein levels were substantially elevated in both SHR groups with higher Trpc6 mRNA expression in SHR-NE. Conclusions: The Wnt/β-catenin and TRPC6/CaN/NFAT hypertrophic signaling pathways seem to be involved in myocardial remodeling in the settings of AH and CKD and might be mediated by FGF23 and α-Klotho axis. Full article
(This article belongs to the Special Issue Molecular Advances in Hypertension and Blood)
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Article
Assessment of Endothelial Injury and Pro-Coagulant Activity Using Circulating Microvesicles in Survivors of Allogeneic Hematopoietic Cell Transplantation
Int. J. Mol. Sci. 2020, 21(24), 9768; https://doi.org/10.3390/ijms21249768 - 21 Dec 2020
Cited by 6 | Viewed by 1059
Abstract
(1) Background: survivors of allogeneic hematopoietic cell transplantation (alloHCT) suffer from morbidity and mortality due to cardiovascular events. We hypothesized that vascular injury and pro-coagulant activity are evident in alloHCT survivors without existing alloHCT complications or relapse. (2) Methods: we enrolled consecutive adult [...] Read more.
(1) Background: survivors of allogeneic hematopoietic cell transplantation (alloHCT) suffer from morbidity and mortality due to cardiovascular events. We hypothesized that vascular injury and pro-coagulant activity are evident in alloHCT survivors without existing alloHCT complications or relapse. (2) Methods: we enrolled consecutive adult alloHCT survivors without established cardiovascular disease and control individuals matched for traditional cardiovascular risk factors (January–December 2019). Circulating microvesicles (MVs) of different cellular origins (platelet, erythrocyte, and endothelial) were measured by a standardized flow cytometry protocol as novel markers of vascular injury and pro-coagulant activity. (3) Results: we recruited 45 survivors after a median of 2.3 (range 1.1–13.2) years from alloHCT, and 45 controls. The majority of patients suffered from acute (44%) and/or chronic (66%) graft-versus-host disease (GVHD). Although the two groups were matched for traditional cardiovascular risk factors, alloHCT survivors showed significantly increased platelet and erythrocyte MVs compared to controls. Within alloHCT survivors, erythrocyte MVs were significantly increased in patients with a previous history of thrombotic microangiopathy. Interestingly, endothelial MVs were significantly increased only in alloHCT recipients of a myeloablative conditioning. Furthermore, MVs of different origins showed a positive association with each other. (4) Conclusions: endothelial dysfunction and increased thrombotic risk are evident in alloHCT recipients long after alloHCT, independently of traditional cardiovascular risk factors. An apparent synergism of these pathophysiological processes may be strongly involved in the subsequent establishment of cardiovascular disease. Full article
(This article belongs to the Special Issue Molecular Advances in Hypertension and Blood)
Article
Ticagrelor Exerts Immune-Modulatory Effect by Attenuating Neutrophil Extracellular Traps
Int. J. Mol. Sci. 2020, 21(10), 3625; https://doi.org/10.3390/ijms21103625 - 21 May 2020
Cited by 9 | Viewed by 1425
Abstract
Neutrophils through the release of neutrophil extracellular traps (NETs) containing active tissue factor (TF) are key components of thrombo-inflammation. Platelets-neutrophils interplay in ST elevation myocardial infarction (STEMI) promotes NET formation via inorganic polyphosphates (polyP) released by thrombin-activated platelets. NETs, however, are also induced [...] Read more.
Neutrophils through the release of neutrophil extracellular traps (NETs) containing active tissue factor (TF) are key components of thrombo-inflammation. Platelets-neutrophils interplay in ST elevation myocardial infarction (STEMI) promotes NET formation via inorganic polyphosphates (polyP) released by thrombin-activated platelets. NETs, however, are also induced by biomaterials in a platelet-independent manner. Considering the possible pleiotropic effects of Ticagrelor beyond platelet inhibition and the clinical need for novel antithrombotic strategies targeting inflammation, we investigated the effects of Ticagrelor on polyP and stent-induced NETs in STEMI. Neutrophils from healthy individuals and patients receiving Ticagrelor were stimulated with polyP or drug-eluting stents (DES) to produce NETs. To induce TF expression, neutrophils were further incubated with plasma obtained from the infarct-related artery (IRA) of STEMI patients. The effects of Ticagrelor on NETs and TF loading were assessed using fluorescence microscopy, flow cytometry, myeloperoxidase(MPO)/DNA complex ELISA, and a Western blot. Ticagrelor interrupts platelet–neutrophil interaction by attenuating NETs induced by polyP. However, Ticagrelor does not affect polyP secretion from thrombin-activated platelets. Similarly, the intracellular production of TF in neutrophils triggered by IRA plasma is not hindered by Ticagrelor. Furthermore, DES induce NETs and synchronous stimulation with IRA plasma leads to the formation of thrombogenic TF-bearing NETs. Ticagrelor inhibits stent-induced NET release. These findings suggest a novel immune-modulatory effect of Ticagrelor when it attenuates the formation of thrombogenic NETs. Full article
(This article belongs to the Special Issue Molecular Advances in Hypertension and Blood)
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Review

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Review
Toll-Like Receptors in the Pathogenesis of Essential Hypertension. A Forthcoming Immune-Driven Theory in Full Effect
Int. J. Mol. Sci. 2021, 22(7), 3451; https://doi.org/10.3390/ijms22073451 - 26 Mar 2021
Cited by 3 | Viewed by 891
Abstract
Essential hypertension (EH) is a highly heterogenous disease with a complex etiology. Recent evidence highlights the significant contribution of subclinical inflammation, triggered and sustained by excessive innate immune system activation in the pathogenesis of the disease. Toll-like receptors (TLRs) have been implied as [...] Read more.
Essential hypertension (EH) is a highly heterogenous disease with a complex etiology. Recent evidence highlights the significant contribution of subclinical inflammation, triggered and sustained by excessive innate immune system activation in the pathogenesis of the disease. Toll-like receptors (TLRs) have been implied as novel effectors in this inflammatory environment since they can significantly stimulate the production of pro-inflammatory cytokines, the migration and proliferation of smooth muscle cells and the generation of reactive oxygen species (ROS), facilitating a low-intensity inflammatory background that is evident from the very early stages of hypertension. Furthermore, the net result of their activation is oxidative stress, endothelial dysfunction, vascular remodeling, and finally, vascular target organ damage, which forms the pathogenetic basis of EH. Importantly, evidence of augmented TLR expression and activation in hypertension has been documented not only in immune but also in several non-immune cells located in the central nervous system, the kidneys, and the vasculature which form the pathogenetic core systems operating in hypertensive disease. In this review, we will try to highlight the contribution of innate immunity in the pathogenesis of hypertension by clarifying the deleterious role of TLR signaling in promoting inflammation and facilitating hypertensive vascular damage. Full article
(This article belongs to the Special Issue Molecular Advances in Hypertension and Blood)
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