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Medicina
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DNA Damage on Cellular Senescence, Aging and Age-Related Diseases
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DNA Damage on Cellular Senescence, Aging and Age-Related Diseases

A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Genetics and Molecular Medicine".

Deadline for manuscript submissions: closed (10 December 2021) | Viewed by 6368

Special Issue Editors

Dr. Varvara Trachana

E-Mail Website
Guest Editor
Department of Biology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece
Interests: DNA damage; cellular senescence; cell cycle checkpoints; autophagy; age-related disease
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Efstathios S. Gonos

E-Mail Website
Co-Guest Editor
National Hellenic Research Foundation (N.H.R.F.), Institute of Biological Research & Biotechnology (I.B.R.B.), 48 Vas. Constantinou Ave., 11635 Athens, Greece
Interests: cellular senescence; proteasome

Special Issue Information

Dear Colleagues,

Life poses threats to the genome; extrinsic sources as well as intrinsic insults can cause DNA damage. This activates the DNA damage response (DDR) which initially leads to growth arrest. Depending on the amount of damage, this transient arrest may result in permanent cell cycle inhibition, i.e., cellular senescence. The causal correlation between DNA damage and senescence as well as aging is supported by findings on mutations or disrupted expression of DDR genes that often result in premature aging. Additionally, recent advances in identifying senescent cells in vivo indicate that senescent cells accumulate with age, possibly as a result of age-related defects in the immune system. This accumulation—together with the tissue repair capacity decline of senescent progenitor cells—would make aged tissues not only less functional but also more vulnerable to other stressors, which could be the causal factor for the appearance of age-related diseases.

Dr. Varvara Trachana
Prof. Efstathios S. Gonos
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. Medicina is an international peer-reviewed open access monthly 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 1800 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.

Keywords

  • DNA damage
  • DNA damage response (DDR)
  • Cellular senescence
  • Aging
  • Age-related diseases

Published Papers (2 papers)

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Research

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16 pages, 2739 KiB  
Article
Dual Role of SIRT1 in Autophagy and Lipid Metabolism Regulation in Osteoarthritic Chondrocytes
by Aliki-Alexandra Papageorgiou, Andreas Goutas, Varvara Trachana and Aspasia Tsezou
Medicina 2021, 57(11), 1203; https://0-doi-org.brum.beds.ac.uk/10.3390/medicina57111203 - 04 Nov 2021
Cited by 11 | Viewed by 2475
Abstract
Background and Objectives: Osteoarthritis (OA) is one of the most common and highly prevalent types of arthritis, also considered a multiphenotypic disease with a strong metabolic component. Ageing is the primary risk factor for OA, while the age-related decline in autophagic activity [...] Read more.
Background and Objectives: Osteoarthritis (OA) is one of the most common and highly prevalent types of arthritis, also considered a multiphenotypic disease with a strong metabolic component. Ageing is the primary risk factor for OA, while the age-related decline in autophagic activity affects cell function and chondrocyte homeostasis. The aim of this study was to investigate the role of sirtuin 1 (SIRT1) in autophagy dysregulation and lipid metabolism in human OA chondrocytes. Materials and Methods: OA chondrocytes were treated with Resveratrol, Hydroxycloroquine (HCQ) or 3-Methyladenine (3-MA) and HCQ or 3-MA followed by siRNA against SIRT1 (siSIRT1). Then, SIRT1, AcNF-κBp65, LOX-1 and autophagy-related proteins ATG5, ATG13, PI3K class III, Beclin-1, LC3 and ULK protein levels were evaluated using Western blot. Normal articular chondrocytes were treated under serum starvation and/or siSIRT1, and the protein expression levels of the above autophagy-related proteins were evaluated. The staining patterns of LC3/p62 and LOX-1 were analyzed microscopically by immunofluorescence. SIRT1/LC3 complex formation was analyzed by immunoprecipitation. Results: SIRT1 and LOX-1 protein expression were negatively correlated in OA chondrocytes. SIRT1 regulated LOX-1 expression via NF-κΒ deacetylation, while treatment with Resveratrol enhanced SIRT1 enzymatic activity, resulting in LOX-1 downregulation and autophagy induction. In OA chondrocytes, SIRT1 was recognized as an autophagy substrate, formed a complex with LC3 and was consequently subjected to cytoplasmic autophagosome-lysosome degradation. Moreover, siSIRT1-treated normal chondrocytes showed decreased autophagic activity, while double-treated (siSIRT1 and serum starvation) cells showed no induction of autophagy. Conclusions: Our results suggest that SIRT1 regulates lipid homeostasis through LOX-1 expression regulation. Additionally, we indicate that the necessity of SIRT1 for autophagy induction in normal chondrocytes, together with its selective autophagic degradation in OA chondrocytes, could contribute to autophagy dysregulation in OA. We, therefore, suggest a novel regulatory scheme that functionally connects lipid metabolism and autophagy in late-stage OA. Full article
(This article belongs to the Special Issue DNA Damage on Cellular Senescence, Aging and Age-Related Diseases)
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Review

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15 pages, 393 KiB  
Review
Mesenchymal Stem Cell Senescence and Osteogenesis
by Artaria Tjempakasari, Heri Suroto and Djoko Santoso
Medicina 2022, 58(1), 61; https://0-doi-org.brum.beds.ac.uk/10.3390/medicina58010061 - 31 Dec 2021
Cited by 8 | Viewed by 3440
Abstract
Mesenchymal stem cells (MSCs) are stem cells with the potential ability to differentiate into various cells and the ability to self-renew and resemble fibroblasts. These cells can adhere to plastic to facilitate the culture process. MSCs can be used in research into tissue [...] Read more.
Mesenchymal stem cells (MSCs) are stem cells with the potential ability to differentiate into various cells and the ability to self-renew and resemble fibroblasts. These cells can adhere to plastic to facilitate the culture process. MSCs can be used in research into tissue biotechnology and rejuvenation medicine. MSCs are also beneficial in recipient tissue and differentiate as a breakthrough strategy through paracrine activity. Many databases have shown MSC-based treatment can be beneficial in the reduction of osteogenesis induced by senescence. In this article, we will discuss the potential effect of MSCs in senescence cells related to osteogenesis. Full article
(This article belongs to the Special Issue DNA Damage on Cellular Senescence, Aging and Age-Related Diseases)
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