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Molecular Advances in Ageing-Related Cardiovascular Diseases
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Molecular Advances in Ageing-Related Cardiovascular Diseases

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 (31 January 2024) | Viewed by 2370

Special Issue Editor

Prof. Dr. Yu Wang

E-Mail Website
Guest Editor
The State Key Laboratory of Pharmaceutical Biotechnology, Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong SAR, China
Interests: proteomics; ageing; obesity; cardiometabolic syndrome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Arterial ageing represents a fundamental cause of all age-related diseases in human. To understand the process and mechanisms of arterial ageing will lead to discoveries of therapeutic agents for keeping the arteries young, in turn preventing age-related diseases. Endothelial cells are the innermost layer of the arterial wall, sense the hemodynamic and humoral microenvironment in the blood, and deliver signals to smooth muscle for modulating the vascular tone responses. Endothelial senescence represents a key characteristic of early vascular aging and contributes to the development of various arterial abnormalities associated with age, such as increased stiffness, calcification, aneurysm and atherosclerosis. The special issue aims to introduce current knowledge, frontier technologies and multidisciplinary applications on arterial ageing.

Topics include:

  • signaling pathways and mechanisms underlying the senescence of endothelial cells
  • structural and functional abnormalities of aged artery
  • cross-talk between different types of cells within the arterial wall
  • strategies for preventing and reverting endothelial senescence and arterial ageing

Prof. Dr. Yu Wang
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.

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

  • cardiovascular diseases
  • arterial ageing
  • vascular ageing
  • endothelial senescence
  • endothelial cells
  • arterial wall
  • vascular tone
  • cell signaling pathway
  • age-related diseases
  • arterial diseases

Published Papers (2 papers)

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Research

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15 pages, 13140 KiB  
Article
Upregulation of Orai Channels Contributes to Aging-Related Vascular Alterations in Rat Coronary Arteries
by Javier Angulo, Argentina Fernández, Alejandro Sevilleja-Ortiz, Alberto Sánchez-Ferrer, Leocadio Rodríguez-Mañas and Mariam El Assar
Int. J. Mol. Sci. 2023, 24(17), 13402; https://doi.org/10.3390/ijms241713402 - 29 Aug 2023
Cited by 1 | Viewed by 863
Abstract
Vascular territories display heterogeneous sensitivity to the impacts of aging. The relevance of the STIM/Orai system to vascular function depends on the vascular bed. We aimed to evaluate the contribution of the STIM/Orai system to aging-related vascular dysfunction in rat coronary circulation. Vascular [...] Read more.
Vascular territories display heterogeneous sensitivity to the impacts of aging. The relevance of the STIM/Orai system to vascular function depends on the vascular bed. We aimed to evaluate the contribution of the STIM/Orai system to aging-related vascular dysfunction in rat coronary circulation. Vascular function was evaluated according to myography in coronary arteries from young (three-month-old) and older (twenty-month-old) rats. The effects of aging and STIM/Orai inhibition on the contraction and relaxation of the coronary arteries and on the protein expression of STIM-1, Orai1, and Orai3 in these vessels were determined. Aging-related hypercontractility to serotonin and endothelin-1 in arteries from male rats was reversed by STIM/Orai inhibition with YM-58483 or by specifically blocking the Orai1 channel with Synta66. The inhibitory effects of Synta66 on coronary vasoconstriction were also observed in older female rats. YM-58483 relaxed serotonin- but not KCl-contracted arteries from males. STIM/Orai inhibition improved defective endothelial vasodilations in aged arteries, even in the presence of NO synthase and cyclooxygenase inhibitors, but not in KCl-contracted segments. YM-58483 significantly enhanced relaxations to calcium-activated potassium channel stimulation in aged vessels. Increased protein expression of Orai1 and Orai3 was detected in arterial homogenates and sections from older rats. Upregulation of the Orai channel contributes to aging-related coronary dysfunction, revealing a potential target in reducing CVD risk. Full article
(This article belongs to the Special Issue Molecular Advances in Ageing-Related Cardiovascular Diseases)
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Review

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22 pages, 1596 KiB  
Review
Functional, Structural and Proteomic Effects of Ageing in Resistance Arteries
by Lars Jørn Jensen
Int. J. Mol. Sci. 2024, 25(5), 2601; https://doi.org/10.3390/ijms25052601 - 23 Feb 2024
Viewed by 1107
Abstract
The normal ageing process affects resistance arteries, leading to various functional and structural changes. Systolic hypertension is a common occurrence in human ageing, and it is associated with large artery stiffening, heightened pulsatility, small artery remodeling, and damage to critical microvascular structures. Starting [...] Read more.
The normal ageing process affects resistance arteries, leading to various functional and structural changes. Systolic hypertension is a common occurrence in human ageing, and it is associated with large artery stiffening, heightened pulsatility, small artery remodeling, and damage to critical microvascular structures. Starting from young adulthood, a progressive elevation in the mean arterial pressure is evidenced by clinical and epidemiological data as well as findings from animal models. The myogenic response, a protective mechanism for the microcirculation, may face disruptions during ageing. The dysregulation of calcium entry channels (L-type, T-type, and TRP channels), dysfunction in intracellular calcium storage and extrusion mechanisms, altered expression of potassium channels, and a change in smooth muscle calcium sensitization may contribute to the age-related dysregulation of myogenic tone. Flow-mediated vasodilation, a hallmark of endothelial function, is compromised in ageing. This endothelial dysfunction is related to increased oxidative stress, lower nitric oxide bioavailability, and a low-grade inflammatory response, further exacerbating vascular dysfunction. Resistance artery remodeling in ageing emerges as a hypertrophic response of the vessel wall that is typically observed in conjunction with outward remodeling (in normotension), or as inward hypertrophic remodeling (in hypertension). The remodeling process involves oxidative stress, inflammation, reorganization of actin cytoskeletal components, and extracellular matrix fiber proteins. Reactive oxygen species (ROS) signaling and chronic low-grade inflammation play substantial roles in age-related vascular dysfunction. Due to its role in the regulation of vascular tone and structural proteins, the RhoA/Rho-kinase pathway is an important target in age-related vascular dysfunction and diseases. Understanding the intricate interplay of these factors is crucial for developing targeted interventions to mitigate the consequences of ageing on resistance arteries and enhance the overall vascular health. Full article
(This article belongs to the Special Issue Molecular Advances in Ageing-Related Cardiovascular Diseases)
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