Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 5857

Share This Special Issue

Special Issue Editor

Prof. Dr. Darío Acuña-Castroviejo

E-Mail Website
Guest Editor

Centro de Investigación Biomédica, Instituto de Biotecnología, Parque Tecnológico de Ciencias de la Salud, Universidad de Granada, 18016 Granada, Spain
Interests: melatonin; mitochondria; aging; neurodegeneration; sepsis; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is the gradual deterioration of functional integrity and systemic homeostasis, concluding in death. During the last century, improvements in health care have notably increased the quality and expectancy of life in humans, but have consequently led to frailty and morbidity. The complexity of aging is determined by the following hallmarks: chronodisruption, genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Advances in research have facilitated the identification of genes that regulate aging, such as those implicated in the molecular machinery of the biological clock, nutrient-sensing pathways, growth factor pathways, mitochondria function, inflammation, and the immune system. Human genetic studies, genetically modified mouse models, and studies on the evolution of lifespan in nature have revealed new avenues to understand the molecular genetics of aging. However, genetic regulation of the elderly remains inscrutable. Furthermore, differences in sex and environmental influences remain unknown and are future challenges within the scientific community. Elucidating the genetic mechanisms that underlie aging is essential for mitigating age-related diseases, reducing fragility, and promoting a healthy human lifespan.

This Special Issue, “Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches”, will discuss the current state of the art, challenges, and opportunities in the field of molecular genetics of aging. Authors are encouraged to submit original research manuscripts and related review articles.

Prof. Dr. Darío Acuña-Castroviejo
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

human aging
molecular clock
aging genes
epigenetics
nutrigenomics
inflammaging
stem cells
telomeres
mitochondria

Published Papers (3 papers)

Download All Papers

Research

Jump to: Review

10 pages, 1497 KiB

Open AccessArticle

Telomere Length, Mitochondrial DNA, and Micronucleus Yield in Response to Oxidative Stress in Peripheral Blood Mononuclear Cells

by Andrea Borghini, Rudina Ndreu, Paola Canale, Jonica Campolo, Irene Marinaro, Antonella Mercuri, Stefano Turchi and Maria Grazia Andreassi

Int. J. Mol. Sci. 2024, 25(3), 1428; https://doi.org/10.3390/ijms25031428 - 24 Jan 2024

Cited by 1 | Viewed by 732

Abstract

Telomere shortening, chromosomal damage, and mitochondrial dysfunction are major initiators of cell aging and biomarkers of many diseases. However, the underlying correlations between nuclear and mitochondrial DNA alterations remain unclear. We investigated the relationship between telomere length (TL) and micronucleus (MN) and their association with mitochondrial DNA copy number (mtDNAcn) in peripheral blood mononuclear cells (PBMCs) in response to 100 μM and 200 μM of hydrogen peroxide (H₂O₂) at 44, 72, and 96 h. Significant TL shortening was observed after both doses of H₂O₂ and at all times (all p < 0.05). A concomitant increase in MN was found at 72 h (p < 0.01) and persisted at 96 h (p < 0.01). An increase in mtDNAcn (p = 0.04) at 200 µM of H₂O₂ was also found. In PBMCs treated with 200 µM H₂O₂, a significant inverse correlation was found between TL and MN (r = −0.76, p = 0.03), and mtDNA content was directly correlated with TL (r = 0.6, p = 0.04) and inversely related to MN (r = −0.78, p = 0.02). Telomere shortening is the main triggering mechanism of chromosomal damage in stimulated T lymphocytes under oxidative stress. The significant correlations between nuclear DNA damage and mtDNAcn support the notion of a telomere–mitochondria axis that might influence age-associated pathologies and be a target for the development of relevant anti-aging drugs. Full article

(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches)

► Show Figures

Figure 1

29 pages, 3398 KiB

Open AccessArticle

Risk Polymorphisms of FNDC5, BDNF, and NTRK2 and Poor Education Interact and Aggravate Age-Related Cognitive Decline

by Alessandra Mendonça Tomás, Natáli Valim Oliver Bento-Torres, Naina Yuki Vieira Jardim, Patrícia Martins Moraes, Victor Oliveira da Costa, Antônio Conde Modesto, André Salim Khayat, João Bento-Torres and Cristovam Wanderley Picanço-Diniz

Int. J. Mol. Sci. 2023, 24(24), 17210; https://doi.org/10.3390/ijms242417210 - 07 Dec 2023

Viewed by 669

Abstract

Cognitive abilities tend to decline with aging, with variation between individuals, and many studies seek to identify genetic biomarkers that more accurately anticipate risks related to pathological aging. We investigated the influence of BDNF, NTRK2, and FNDC5 single nucleotide polymorphisms (SNPs) on the cognitive performance of young and older adults with contrasting educational backgrounds. We addressed three questions: (1) Is education associated with reduced age-related cognitive decline? (2) Does the presence of SNPs explain the variation in cognitive performance observed late in life? (3) Is education differentially associated with cognition based on the presence of BDNF, NTRK2, or FNDC5 polymorphisms? We measured the cognitive functions of young and older participants, with lower and higher education, using specific and sensitive tests of the Cambridge Automated Neuropsychological Test Assessment Battery. A three-way ANOVA revealed that SNPs were associated with differential performances in executive functions, episodic memory, sustained attention, mental and motor response speed, and visual recognition memory and that higher educational levels improved the affected cognitive functions. The results revealed that distinct SNPs affect cognition late in life differentially, suggesting their utility as potential biomarkers and emphasizing the importance of cognitive stimulation that advanced education early in life provides. Full article

(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches)

► Show Figures

Figure 1

Review

Jump to: Research

28 pages, 816 KiB

Open AccessReview

Genomic Instability and Epigenetic Changes during Aging

by Lucía López-Gil, Amparo Pascual-Ahuir and Markus Proft

Int. J. Mol. Sci. 2023, 24(18), 14279; https://doi.org/10.3390/ijms241814279 - 19 Sep 2023

Cited by 4 | Viewed by 3758

Abstract

Aging is considered the deterioration of physiological functions along with an increased mortality rate. This scientific review focuses on the central importance of genomic instability during the aging process, encompassing a range of cellular and molecular changes that occur with advancing age. In particular, this revision addresses the genetic and epigenetic alterations that contribute to genomic instability, such as telomere shortening, DNA damage accumulation, and decreased DNA repair capacity. Furthermore, the review explores the epigenetic changes that occur with aging, including modifications to histones, DNA methylation patterns, and the role of non-coding RNAs. Finally, the review discusses the organization of chromatin and its contribution to genomic instability, including heterochromatin loss, chromatin remodeling, and changes in nucleosome and histone abundance. In conclusion, this review highlights the fundamental role that genomic instability plays in the aging process and underscores the need for continued research into these complex biological mechanisms. Full article

(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches)

► Show Figures