10th Anniversary of Cells—Advances in Cellular and Organismal Aging

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (15 October 2021) | Viewed by 25354

Special Issue Editors


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Guest 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

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Guest Editor
Friedrich Schiller Universitat Jena, Institute of Biochemistry and Biophysics, Jena, Germany
Interests: epigenetics; long-noncoding RNA; transcription, nucleolus; aging; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The year 2021 marks the 10th anniversary since the inaugural issue of Cells was published. We are delighted and proud to celebrate this occasion with a series of Special Issues and events. To date, the journal has published more than 4000 papers, and the journal website attracts more than 50,000 monthly page views. We would like to express our sincerest gratitude to our readers, innumerable authors, peer reviewers, editors, and all the people who have made substantial contributions to the journal’s success over the years. Without your support, we would never have made it.

To mark this important milestone in the topic section “Cellular Aging”, a Special Issue entitled “10th Anniversary of Cells—Advances in Cellular and Organismal Aging” is being launched. This Special Issue invites research articles and high-quality review papers focusing on molecular mechanisms and pathways inherently connected with cellular and organismal aging. We kindly encourage researchers working on aging and related areas including, but not limited to, stem cell biology, senescence, epigenetics, genome stability, protein quality control, metabolism, regeneration, and aging clocks to make contributions to this Special Issue.

This scientific journal is the collaborative achievement of many scientists from all over the world, and we would like to thank all our authors and reviewers who have contributed to this Special Issue. In recognition of our authors’ continued support, Cells is pleased to announce that the Cells Best Paper Awards for Anniversary Special Issues will be launched and granted to the best papers published in the Anniversary Special Issues. See the details at the following link:

https://www.mdpi.com/journal/cells/awards

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Prof. Dr. Christoph Englert
Dr. Holger Bierhoff
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. 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 (4 papers)

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Review

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10 pages, 888 KiB  
Review
The Potentials of Methylene Blue as an Anti-Aging Drug
by Huijing Xue, Abhirami Thaivalappil and Kan Cao
Cells 2021, 10(12), 3379; https://doi.org/10.3390/cells10123379 - 01 Dec 2021
Cited by 14 | Viewed by 14317
Abstract
Methylene blue (MB), as the first fully man-made medicine, has a wide range of clinical applications. Apart from its well-known applications in surgical staining, malaria, and methemoglobinemia, the anti-oxidative properties of MB recently brought new attention to this century-old drug. Mitochondrial dysfunction has [...] Read more.
Methylene blue (MB), as the first fully man-made medicine, has a wide range of clinical applications. Apart from its well-known applications in surgical staining, malaria, and methemoglobinemia, the anti-oxidative properties of MB recently brought new attention to this century-old drug. Mitochondrial dysfunction has been observed in systematic aging that affects many different tissues, including the brain and skin. This leads to increaseding oxidative stress and results in downstream phenotypes under age-related conditions. MB can bypass Complex I/III activity in mitochondria and diminish oxidative stress to some degree. This review summarizes the recent studies on the applications of MB in treating age-related conditions, including neurodegeneration, memory loss, skin aging, and a premature aging disease, progeria. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular and Organismal Aging)
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18 pages, 3671 KiB  
Review
Multifunctionality of the Telomere-Capping Shelterin Complex Explained by Variations in Its Protein Composition
by Claire Ghilain, Eric Gilson and Marie-Josèphe Giraud-Panis
Cells 2021, 10(7), 1753; https://doi.org/10.3390/cells10071753 - 11 Jul 2021
Cited by 15 | Viewed by 4598
Abstract
Protecting telomere from the DNA damage response is essential to avoid the entry into cellular senescence and organismal aging. The progressive telomere DNA shortening in dividing somatic cells, programmed during development, leads to critically short telomeres that trigger replicative senescence and thereby contribute [...] Read more.
Protecting telomere from the DNA damage response is essential to avoid the entry into cellular senescence and organismal aging. The progressive telomere DNA shortening in dividing somatic cells, programmed during development, leads to critically short telomeres that trigger replicative senescence and thereby contribute to aging. In several organisms, including mammals, telomeres are protected by a protein complex named Shelterin that counteract at various levels the DNA damage response at chromosome ends through the specific function of each of its subunits. The changes in Shelterin structure and function during development and aging is thus an intense area of research. Here, we review our knowledge on the existence of several Shelterin subcomplexes and the functional independence between them. This leads us to discuss the possibility that the multifunctionality of the Shelterin complex is determined by the formation of different subcomplexes whose composition may change during aging. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular and Organismal Aging)
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28 pages, 2396 KiB  
Review
An Analysis of the Neurological and Molecular Alterations Underlying the Pathogenesis of Alzheimer’s Disease
by Chantal Vidal and Li Zhang
Cells 2021, 10(3), 546; https://doi.org/10.3390/cells10030546 - 04 Mar 2021
Cited by 11 | Viewed by 3498
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by amyloid beta (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Unfortunately, despite decades of studies being performed on these histological alterations, there is no effective treatment or cure for AD. Identifying the molecular characteristics of [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by amyloid beta (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Unfortunately, despite decades of studies being performed on these histological alterations, there is no effective treatment or cure for AD. Identifying the molecular characteristics of the disease is imperative to understanding the pathogenesis of AD. Furthermore, uncovering the key causative alterations of AD can be valuable in developing models for AD treatment. Several alterations have been implicated in driving this disease, including blood–brain barrier dysfunction, hypoxia, mitochondrial dysfunction, oxidative stress, glucose hypometabolism, and altered heme homeostasis. Although these alterations have all been associated with the progression of AD, the root cause of AD has not been identified. Intriguingly, recent studies have pinpointed dysfunctional heme metabolism as a culprit of the development of AD. Heme has been shown to be central in neuronal function, mitochondrial respiration, and oxidative stress. Therefore, dysregulation of heme homeostasis may play a pivotal role in the manifestation of AD and its various alterations. This review will discuss the most common neurological and molecular alterations associated with AD and point out the critical role heme plays in the development of this disease. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular and Organismal Aging)
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6 pages, 731 KiB  
Commentary
Age-Dependent Microglial Response to Systemic Infection
by Brianna Cyr and Juan Pablo de Rivero Vaccari
Cells 2021, 10(5), 1037; https://doi.org/10.3390/cells10051037 - 28 Apr 2021
Cited by 3 | Viewed by 1915
Abstract
Inflammation is part of the aging process, and the inflammatory innate immune response is more exacerbated in older individuals when compared to younger individuals. Similarly, there is a difference in the response to systemic infection that varies with age. In a recent article [...] Read more.
Inflammation is part of the aging process, and the inflammatory innate immune response is more exacerbated in older individuals when compared to younger individuals. Similarly, there is a difference in the response to systemic infection that varies with age. In a recent article by Hoogland et al., the authors studied the microglial response to systemic infection in young (2 months) and middle-aged mice (13–14 months) that were challenged with live Escherichia coli to investigate whether the pro- and anti-inflammatory responses mounted by microglia after systemic infection varies with age. Here, we comment on this study and its implications on how inflammation in the brain varies with age. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular and Organismal Aging)
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