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From Ageing and Vascular Ageing to Specific Treatment of Age-Related Disorders

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: closed (31 July 2021) | Viewed by 7964

Special Issue Editor

Dr. Miso Sabovic

E-Mail Website
Guest Editor
Department of Vascular Diseases, Ljubljana University Medical Centre, Zaloška cesta 7, SI-1000 Ljubljana, Slovenia
Interests: atherosclerosis; ageing; ageing of cardiovascular system; arterial wall; arterial stiffness; cardiovascular prevention; diabetes; endothelial dysfunction; lipids; metabolic syndrome

Special Issue Information

Dear Colleagues,

The global population is progressively ageing, and therefore the rate of elderly individuals with age-related disorders such as cardio-vascular disorders, neurodegenerative disorders, and carcinoma has been enormously increased. Along with classical management of these diseases, effective “ageing-specific” prevention and/or treatment would be of paramount interest to achieve “healthy ageing”, which is already one of the priorities of our society. At least in theory, the treatment can be assisted or even led by the approaches developed by knowledge from basic ageing research.  Whereas whole-body ageing is still poorly explained, much more is known about specific tissue/organ ageing, as best represented by vascular ageing. Overall, it seems to be a promising approach to manage ageing-related disorders by translating unspecific ageing research into specific clinical interventions. Thus, the aim of the present Special Issue entitled “From Ageing and Vascular Ageing to Specific Treatment of Age-Related Disorders” is to describe the knowledge from the ageing research field that has the potential for the prevention and/or treatment of age-related disorders. The description and rationale of knowledge possibly translated from bench (ageing and vascular ageing research) to bed (age-related disorders), although possibly still speculative or unconfirmed, could in future lead to new effective clinical approaches.

Dr. Miso Sabovic
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

  • ageing
  • vascular ageing
  • age-related disorders
  • prevention
  • treatment
  • healthy ageing
  • pathophysiology
  • innovation
  • new approach

Published Papers (3 papers)

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Research

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17 pages, 3179 KiB  
Article
Discoidin Domain Receptor 2 Regulates AT1R Expression in Angiotensin II-Stimulated Cardiac Fibroblasts via Fibronectin-Dependent Integrin-β1 Signaling
by Allen Sam Titus, Harikrishnan Venugopal, Mereena George Ushakumary, Mingyi Wang, Randy T. Cowling, Edward G. Lakatta and Shivakumar Kailasam
Int. J. Mol. Sci. 2021, 22(17), 9343; https://doi.org/10.3390/ijms22179343 - 28 Aug 2021
Cited by 7 | Viewed by 2361
Abstract
This study probed the largely unexplored regulation and role of fibronectin in Angiotensin II-stimulated cardiac fibroblasts. Using gene knockdown and overexpression approaches, Western blotting, and promoter pull-down assay, we show that collagen type I-activated Discoidin Domain Receptor 2 (DDR2) mediates Angiotensin II-dependent transcriptional [...] Read more.
This study probed the largely unexplored regulation and role of fibronectin in Angiotensin II-stimulated cardiac fibroblasts. Using gene knockdown and overexpression approaches, Western blotting, and promoter pull-down assay, we show that collagen type I-activated Discoidin Domain Receptor 2 (DDR2) mediates Angiotensin II-dependent transcriptional upregulation of fibronectin by Yes-activated Protein in cardiac fibroblasts. Furthermore, siRNA-mediated fibronectin knockdown attenuated Angiotensin II-stimulated expression of collagen type I and anti-apoptotic cIAP2, and enhanced cardiac fibroblast susceptibility to apoptosis. Importantly, an obligate role for fibronectin was observed in Angiotensin II-stimulated expression of AT1R, the Angiotensin II receptor, which would link extracellular matrix (ECM) signaling and Angiotensin II signaling in cardiac fibroblasts. The role of fibronectin in Angiotensin II-stimulated cIAP2, collagen type I, and AT1R expression was mediated by Integrin-β1-integrin-linked kinase signaling. In vivo, we observed modestly reduced basal levels of AT1R in DDR2-null mouse myocardium, which were associated with the previously reported reduction in myocardial Integrin-β1 levels. The role of fibronectin, downstream of DDR2, could be a critical determinant of cardiac fibroblast-mediated wound healing following myocardial injury. In summary, our findings suggest a complex mechanism of regulation of cardiac fibroblast function involving two major ECM proteins, collagen type I and fibronectin, and their receptors, DDR2 and Integrin-β1. Full article
(This article belongs to the Special Issue From Ageing and Vascular Ageing to Specific Treatment of Age-Related Disorders)
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12 pages, 1813 KiB  
Article
Post-Stroke Social Isolation Reduces Cell Proliferation in the Dentate Gyrus and Alters miRNA Profiles in the Aged Female Mice Brain
by Aleah Holmes, Yan Xu, Juneyoung Lee, Michael E. Maniskas, Liang Zhu, Louise D. McCullough and Venugopal Reddy Venna
Int. J. Mol. Sci. 2021, 22(1), 99; https://doi.org/10.3390/ijms22010099 - 24 Dec 2020
Cited by 7 | Viewed by 2332
Abstract
Social isolation and loneliness are risk factors for stroke. Elderly women are more likely to be isolated. Census data shows that in homeowners over the age of 65, women are much more likely to live alone. However, the underlying mechanisms of the detrimental [...] Read more.
Social isolation and loneliness are risk factors for stroke. Elderly women are more likely to be isolated. Census data shows that in homeowners over the age of 65, women are much more likely to live alone. However, the underlying mechanisms of the detrimental effects of isolation have not been well studied in older females. In this study, we hypothesized that isolation impairs post-stroke recovery in aged female mice, leading to dysregulated microRNAs (miRNAs) in the brain, including those previously shown to be involved in response to social isolation (SI). Aged C57BL/6 female mice were subjected to a 60-min middle cerebral artery occlusion and were randomly assigned to either single housing (SI) or continued pair housing (PH) immediately after stroke for 15 days. SI immediately after stroke led to significantly more brain tissue loss after stroke and higher mortality. Furthermore, SI significantly delayed motor and sensory recovery and worsened cognitive function, compared to PH. A decrease in cell proliferation was seen in the dentate gyrus of SI mice assessed by bromodeoxyuridine (BrdU) labeling. miRNAome data analysis revealed changes in several miRNAs in the brain, such as miR-297a-3p and miR-200c-3p, which are known to regulate pathways involved in cell proliferation. In conclusion, our data suggest that SI can lead to a poor post-stroke recovery in aged females and dysregulation of miRNAs and reduced hippocampal cell proliferation. Full article
(This article belongs to the Special Issue From Ageing and Vascular Ageing to Specific Treatment of Age-Related Disorders)
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Review

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16 pages, 1518 KiB  
Review
Treating Arterial Ageing in Patients with Diabetes: From Mechanisms to Effective Drugs
by Mojca Lunder, Miodrag Janić and Mišo Šabovič
Int. J. Mol. Sci. 2021, 22(6), 2796; https://doi.org/10.3390/ijms22062796 - 10 Mar 2021
Cited by 9 | Viewed by 2571
Abstract
Diabetes mellitus is a major healthcare problem. It is not only characterized by hyperglycemia and chronic complications, but in longer lasting diabetes and a longer living population, it is also associated with accelerated arterial ageing, which importantly contributes to cardiovascular complications. The accelerated [...] Read more.
Diabetes mellitus is a major healthcare problem. It is not only characterized by hyperglycemia and chronic complications, but in longer lasting diabetes and a longer living population, it is also associated with accelerated arterial ageing, which importantly contributes to cardiovascular complications. The accelerated arterial ageing in patients with diabetes should be considered separately from arterial ageing in patients without diabetes. Basic and clinical research have allowed better insight into the mechanisms of arterial ageing. In a simplified mechanistic way, it could be considered that the three tightly connected cornerstone characteristics of arterial ageing in patients with diabetes are: phenotypic presentation as endothelial dysfunction and arterial stiffness, and the underlying basic ageing-facilitating mechanism represented as the impaired expression of genetic longevity pathways. Currently, specific drugs for preventing/treating arterial ageing are not available. Therefore, we aimed to review the capacity of available drugs, particularly antidiabetic drugs, to interfere with the arterial ageing process. In the near future, these characteristics could help to guide therapy in patients with diabetes. Overall, it appears that arterial ageing could become a new target in diabetes. The expanding knowledge regarding the capability of antidiabetic drugs and other available drugs to inhibit/delay arterial aging is therefore essential. Full article
(This article belongs to the Special Issue From Ageing and Vascular Ageing to Specific Treatment of Age-Related Disorders)
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