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Age-Related Vascular Physiology
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Age-Related Vascular Physiology

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 (30 June 2024) | Viewed by 5026

Special Issue Editor

Dr. Maurizio Mandalà

E-Mail Website
Guest Editor
Department of Biology, Ecology and Earth Sciences, University of Calabria, 87036 Rende, Italy
Interests: arteries; veins; hypertension; vascular remodeling; pregnancy; preeclampsia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Blood vessels play a crucial role in the proper function of the organs and the well-being of the organism. Age changes in the vasculature are associated with vascular diseases that lead to significant morbidity and mortality of old people, which are ever increasing in the population, and primary care is a priority for clinicians.

One common factor to this health issue is an age-related decline in vascular structure and function that is presently not completely understood. Several studies are focused on understanding molecular aspects of age-impaired vascular systems. This Special Issue aims to collect the most recent information related to vascular changes associated with aging and the underlying molecular mechanisms to provide new insights and innovative strategies for the management of vascular disorders that affect older people.

Dr. Maurizio Mandalà
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 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.

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Keywords

  • aging
  • blood vessels
  • blood flow
  • hemodynamic
  • endothelial cells
  • smooth muscle cells
  • artery
  • veins

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Published Papers (2 papers)

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Research

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12 pages, 2392 KiB  
Article
Epidermal Growth Factor Receptors in Vascular Endothelial Cells Contribute to Functional Hyperemia in the Brain
by Hannah R. Ferris, Nathan C. Stine, David C. Hill-Eubanks, Mark T. Nelson, George C. Wellman and Masayo Koide
Int. J. Mol. Sci. 2023, 24(22), 16284; https://doi.org/10.3390/ijms242216284 - 14 Nov 2023
Cited by 2 | Viewed by 1495
Abstract
Functional hyperemia—activity-dependent increases in local blood perfusion—underlies the on-demand delivery of blood to regions of enhanced neuronal activity, a process that is crucial for brain health. Importantly, functional hyperemia deficits have been linked to multiple dementia risk factors, including aging, chronic hypertension, and [...] Read more.
Functional hyperemia—activity-dependent increases in local blood perfusion—underlies the on-demand delivery of blood to regions of enhanced neuronal activity, a process that is crucial for brain health. Importantly, functional hyperemia deficits have been linked to multiple dementia risk factors, including aging, chronic hypertension, and cerebral small vessel disease (cSVD). We previously reported crippled functional hyperemia in a mouse model of genetic cSVD that was likely caused by depletion of phosphatidylinositol 4,5-bisphosphate (PIP2) in capillary endothelial cells (EC) downstream of impaired epidermal growth factor receptor (EGFR) signaling. Here, using EC-specific EGFR-knockout (KO) mice, we directly examined the role of endothelial EGFR signaling in functional hyperemia, assessed by measuring increases in cerebral blood flow in response to contralateral whisker stimulation using laser Doppler flowmetry. Molecular characterizations showed that EGFR expression was dramatically decreased in freshly isolated capillaries from EC-EGFR-KO mice, as expected. Notably, whisker stimulation-induced functional hyperemia was significantly impaired in these mice, an effect that was rescued by administration of PIP2, but not by the EGFR ligand, HB-EGF. These data suggest that the deletion of the EGFR specifically in ECs attenuates functional hyperemia, likely via depleting PIP2 and subsequently incapacitating Kir2.1 channel functionality in capillary ECs. Thus, our study underscores the role of endothelial EGFR signaling in functional hyperemia of the brain. Full article
(This article belongs to the Special Issue Age-Related Vascular Physiology)
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Review

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32 pages, 2674 KiB  
Review
The Molecular Heterogeneity of Store-Operated Ca2+ Entry in Vascular Endothelial Cells: The Different roles of Orai1 and TRPC1/TRPC4 Channels in the Transition from Ca2+-Selective to Non-Selective Cation Currents
by Francesco Moccia, Valentina Brunetti, Angelica Perna, Germano Guerra, Teresa Soda and Roberto Berra-Romani
Int. J. Mol. Sci. 2023, 24(4), 3259; https://doi.org/10.3390/ijms24043259 - 7 Feb 2023
Cited by 18 | Viewed by 2980
Abstract
Store-operated Ca2+ entry (SOCE) is activated in response to the inositol-1,4,5-trisphosphate (InsP3)-dependent depletion of the endoplasmic reticulum (ER) Ca2+ store and represents a ubiquitous mode of Ca2+ influx. In vascular endothelial cells, SOCE regulates a plethora of functions [...] Read more.
Store-operated Ca2+ entry (SOCE) is activated in response to the inositol-1,4,5-trisphosphate (InsP3)-dependent depletion of the endoplasmic reticulum (ER) Ca2+ store and represents a ubiquitous mode of Ca2+ influx. In vascular endothelial cells, SOCE regulates a plethora of functions that maintain cardiovascular homeostasis, such as angiogenesis, vascular tone, vascular permeability, platelet aggregation, and monocyte adhesion. The molecular mechanisms responsible for SOCE activation in vascular endothelial cells have engendered a long-lasting controversy. Traditionally, it has been assumed that the endothelial SOCE is mediated by two distinct ion channel signalplexes, i.e., STIM1/Orai1 and STIM1/Transient Receptor Potential Canonical 1(TRPC1)/TRPC4. However, recent evidence has shown that Orai1 can assemble with TRPC1 and TRPC4 to form a non-selective cation channel with intermediate electrophysiological features. Herein, we aim at bringing order to the distinct mechanisms that mediate endothelial SOCE in the vascular tree from multiple species (e.g., human, mouse, rat, and bovine). We propose that three distinct currents can mediate SOCE in vascular endothelial cells: (1) the Ca2+-selective Ca2+-release activated Ca2+ current (ICRAC), which is mediated by STIM1 and Orai1; (2) the store-operated non-selective current (ISOC), which is mediated by STIM1, TRPC1, and TRPC4; and (3) the moderately Ca2+-selective, ICRAC-like current, which is mediated by STIM1, TRPC1, TRPC4, and Orai1. Full article
(This article belongs to the Special Issue Age-Related Vascular Physiology)
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