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Collection of Cell Aging—The Road Map of Aging
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Collection of Cell Aging—The Road Map of Aging

A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Cellular Aging".

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Editor

Prof. Dr. Christoph Englert

E-Mail Website
Collection Editor
Leibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany
Interests: regulation of gene expression; development; organogenesis; cellular and organismic aging
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

Aging is accompanied by a continuous decline in the capacity to maintain organ homeostasis and function. At the same time, the median human lifespan continues to increase. Thus, understanding the molecular and cellular mechanisms that underlie the aging process is of significant societal impact and high scientific interest. In recent years, exciting progress has been made regarding several aspects of research on aging, such as senescence, stem cell biology, sex-specific aspects of aging, and epigenetics. Moreover, the reprogramming phenomenon and the development of senolytics have contributed to the vision that a deceleration of at least some aspects of aging might be in sight. 

With this topic collection, we want to cover a wide array of topics, including but not limited to aging-associated changes in the epigenome, the cellular surveillance of protein homeostasis, damage response, cellular senescence, stem cell function and tissue regeneration, the aging of the immune system, the links between metabolism and aging, aging clocks, and aging-associated diseases. We also invite the submission of manuscripts on the translational aspects of research on aging, including those on the development of interventions in model organisms and humans.

Prof. Dr. Christoph Englert
Collection 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 collection 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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 (3 papers)

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2024

Jump to: 2023

11 pages, 3984 KiB  
Article
Role of Piezo1 in Terminal Density Reversal of Red Blood Cells
by Kuntal Dey, Ankie M. van Cromvoirt, Inga Hegemann, Jeroen S. Goede and Anna Bogdanova
Cells 2024, 13(16), 1363; https://doi.org/10.3390/cells13161363 - 16 Aug 2024
Viewed by 658
Abstract
Density reversal of senescent red blood cells has been known for a long time, yet the identity of the candidate ion transporter(s) causing the senescent cells to swell is still elusive. While performing fractionation of RBCs from healthy individuals in Percoll density gradient [...] Read more.
Density reversal of senescent red blood cells has been known for a long time, yet the identity of the candidate ion transporter(s) causing the senescent cells to swell is still elusive. While performing fractionation of RBCs from healthy individuals in Percoll density gradient and characterization of the separated fractions, we identified a subpopulation of cells in low-density fraction (1.02% ± 0.47) showing signs of senescence such as loss of membrane surface area associated with a reduction in band 3 protein abundance, and Phosphatidylserine (PS) exposure to the outer membrane. In addition, we found that these cells are overloaded with Na+ and Ca2+. Using a combination of blockers and activators of ion pumps and channels, we revealed reduced activity of Plasma membrane Ca2+ ATPase and an increase in Ca2+ and Na+ leaks through ion channels in senescent-like cells. Our data revealed that Ca2+ overload in these cells is a result of reduced PMCA activity and facilitated Ca2+ uptake via a hyperactive Piezo1 channel. However, we could not exclude the contribution of other Ca2+-permeable ion channels in this scenario. In addition, we found, as a universal mechanism, that an increase in intracellular Ca2+ reduced the initially high selectivity of Piezo1 channel for Ca2+ and allowed higher Na+ uptake, Na+ accumulation, and swelling. Full article
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19 pages, 6205 KiB  
Article
Cell Senescence-Independent Changes of Human Skin Fibroblasts with Age
by Nicola Fullard, James Wordsworth, Ciaran Welsh, Victoria Maltman, Charlie Bascom, Ryan Tasseff, Robert Isfort, Lydia Costello, Rebekah-Louise Scanlan, Stefan Przyborski and Daryl Shanley
Cells 2024, 13(8), 659; https://doi.org/10.3390/cells13080659 - 9 Apr 2024
Cited by 1 | Viewed by 2698
Abstract
Skin ageing is defined, in part, by collagen depletion and fragmentation that leads to a loss of mechanical tension. This is currently believed to reflect, in part, the accumulation of senescent cells. We compared the expression of genes and proteins for components of [...] Read more.
Skin ageing is defined, in part, by collagen depletion and fragmentation that leads to a loss of mechanical tension. This is currently believed to reflect, in part, the accumulation of senescent cells. We compared the expression of genes and proteins for components of the extracellular matrix (ECM) as well as their regulators and found that in vitro senescent cells produced more matrix metalloproteinases (MMPs) than proliferating cells from adult and neonatal donors. This was consistent with previous reports of senescent cells contributing to increased matrix degradation with age; however, cells from adult donors proved significantly less capable of producing new collagen than neonatal or senescent cells, and they showed significantly lower myofibroblast activation as determined by the marker α-SMA. Functionally, adult cells also showed slower migration than neonatal cells. We concluded that the increased collagen degradation of aged fibroblasts might reflect senescence, the reduced collagen production likely reflects senescence-independent processes. Full article
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2023

Jump to: 2024

19 pages, 1042 KiB  
Article
Effects of an Intervention with Selenium and Coenzyme Q10 on Five Selected Age-Related Biomarkers in Elderly Swedes Low in Selenium: Results That Point to an Anti-Ageing Effect—A Sub-Analysis of a Previous Prospective Double-Blind Placebo-Controlled Randomised Clinical Trial
by Urban Alehagen, Jan Alexander, Jan O. Aaseth, Anders Larsson, Erland Svensson and Trine B. Opstad
Cells 2023, 12(13), 1773; https://doi.org/10.3390/cells12131773 - 4 Jul 2023
Cited by 1 | Viewed by 3092
Abstract
Background: Ageing is associated with cardiovascular disease (CVD). As no single biomarker reflects the full ageing process, we aimed to investigate five CVD- and age-related markers and the effects of selenium and coenzyme Q10 intervention to elucidate the mechanisms that may influence the [...] Read more.
Background: Ageing is associated with cardiovascular disease (CVD). As no single biomarker reflects the full ageing process, we aimed to investigate five CVD- and age-related markers and the effects of selenium and coenzyme Q10 intervention to elucidate the mechanisms that may influence the course of ageing. Methods: This is a sub-study of a previous prospective double-blind placebo-controlled randomized clinical trial that included 441 subjects low in selenium (mean age 77, 49% women). The active treatment group (n = 220) received 200 µg/day of selenium and 200 mg/day of coenzyme Q10, combined. Blood samples were collected at inclusion and after 48 months for measurements of the intercellular adhesion molecule (ICAM-1), adiponectin, leptin, stem cell factor (SCF) and osteoprotegerin (OPG), using ELISAs. Repeated measures of variance and ANCOVA evaluations were used to compare the two groups. In order to better understand and reduce the complexity of the relationship between the biomarkers and age, factor analyses and structural equation modelling (SEM) were performed, and a structural model is presented. Results: Correlation analyses of biomarker values at inclusion in relation to age, and relevant markers related to inflammation, endothelial dysfunction and fibrosis, demonstrated the biomarkers’ association with these pathological processes; however, only ICAM1 and adiponectin were directly correlated with age. SEM analyses showed, however, that the biomarkers ICAM-1, adiponectin, SCF and OPG, but not leptin, all had significant associations with age and formed two independent structural factors, both significantly related to age. While no difference was observed at inclusion, the biomarkers were differently changed in the active treatment and placebo groups (decreasing and increasing levels, respectively) at 48 months (p ≤ 0.02 in all, adjusted), and in the SEM model, they showed an anti-ageing impact. Conclusions: Supplementation with selenium/Q10 influenced the analysed biomarkers in ways indicating an anti-ageing effect, and by applying SEM methodology, the interrelationships between two independent structural factors and age were validated. Full article
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