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Molecular Studies in Aging: New Advances

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 March 2024) | Viewed by 15150

Special Issue Editors


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Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences, University ”G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Interests: oxidative stress and antioxidant enzymes; cellular signalling; growth factors; muscular trophism; muscle and bone stem cells; regenerative aspects of space flight; sarcopenia; regeneration of muscle and bone tissues
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences, University ”G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Interests: muscle stem cells; molecular biology; skeletal muscle regeneration

Special Issue Information

Dear Colleagues,

The perspective regarding the lengthening of life raises the fundamental issue of aging in good health, with autonomy and independence, both for the quality of life and the containment of health care costs. This represents a challenge to maintaining efficient tissues, organs, and systems of the body.
Lifestyle and environmental factors play a preponderant role during the early stages of life, while genetics become fundamental to establish the complete life span of an organism.
Today, several approaches are used to both study and better understand the mechanisms underlying the aging processes, as well as to counteract and decelerate them. There are several tissues and systems that undergo aging, and among those most affected are the muscle, bone, nervous system, and cardiovascular system. The rationale of this Special Issue is essentially to collect new discoveries and study approaches on aging processes at the molecular, cellular, and integrative levels, as well as new proposals for the achievement of active aging (for example, mind training, physical activity, and diet).
For this Special Issue, we invite researchers to provide original research articles and review articles regarding results in the field of the new frontiers that can contribute to the understanding of aging processes and the prospect of healthy old age.

Dr. Stefania Fulle
Dr. Rosa Mancinelli
Guest Editors

Manuscript Submission Information

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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

  • Senescence
  • Active aging
  • Sarcopenia
  • Osteoporosis
  • Oxidative stress
  • Brain aging
  • Cardiovascular aging

Published Papers (5 papers)

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Research

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17 pages, 3152 KiB  
Article
From Immunosenescence to Aging Types—Establishing Reference Intervals for Immune Age Biomarkers by Centile Estimation
by Peter Bröde, Maren Claus, Patrick D. Gajewski, Stephan Getzmann, Edmund Wascher and Carsten Watzl
Int. J. Mol. Sci. 2023, 24(17), 13186; https://doi.org/10.3390/ijms241713186 - 24 Aug 2023
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Abstract
Immunological aging type definition requires establishing reference intervals from the distribution of immunosenescence biomarkers conditional on age. For 1605 individuals (18–97 years), we determined the comprehensive immune age index IMMAX from flow-cytometry-based blood cell sub-populations and identified age-specific centiles by fitting generalized additive [...] Read more.
Immunological aging type definition requires establishing reference intervals from the distribution of immunosenescence biomarkers conditional on age. For 1605 individuals (18–97 years), we determined the comprehensive immune age index IMMAX from flow-cytometry-based blood cell sub-populations and identified age-specific centiles by fitting generalized additive models for location, scale, and shape. The centiles were uncorrelated with age and facilitated the categorization of individuals as immunologically slow or fast aging types. Using its 50th percentile as a reference, we rescaled the IMMAX to equivalent years of life (EYOL) and computed the immunological age gap as the difference between EYOL and chronological age. Applied to preliminary baseline and follow-up measurements from 53 participants of the Dortmund Vital Study (Clinical-Trials.gov Identifier: NCT05155397), the averaged changes in the IMMAX and EYOL conformed to the 5-year follow-up period, whereas no significant changes occurred concerning IMMAX centiles and age gap. This suggested that the participants immunologically adapted to aging and kept their relative positions within the cohort. Sex was non-significant. Methodical comparisons indicated that future confirmatory analyses with the completed follow-up examinations could rely on percentile curves estimated by simple linear quantile regression, while the selection of the immunosenescence biomarker will greatly influence the outcome, with IMMAX representing the preferable choice. Full article
(This article belongs to the Special Issue Molecular Studies in Aging: New Advances)
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Review

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23 pages, 2397 KiB  
Review
Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice
by Andrea Ágnes Molnár, Dorottya Tímea Pásztor, Zsófia Tarcza and Béla Merkely
Int. J. Mol. Sci. 2023, 24(24), 17129; https://doi.org/10.3390/ijms242417129 - 05 Dec 2023
Cited by 1 | Viewed by 1632
Abstract
Aging is a major risk factor of atherosclerosis through different complex pathways including replicative cellular senescence and age-related clonal hematopoiesis. In addition to aging, extracellular stress factors, such as mechanical and oxidative stress, can induce cellular senescence, defined as premature cellular senescence. Senescent [...] Read more.
Aging is a major risk factor of atherosclerosis through different complex pathways including replicative cellular senescence and age-related clonal hematopoiesis. In addition to aging, extracellular stress factors, such as mechanical and oxidative stress, can induce cellular senescence, defined as premature cellular senescence. Senescent cells can accumulate within atherosclerotic plaques over time and contribute to plaque instability. This review summarizes the role of cellular senescence in the complex pathophysiology of atherosclerosis and highlights the most important senotherapeutics tested in cardiovascular studies targeting senescence. Continued bench-to-bedside research in cellular senescence might allow the future implementation of new effective anti-atherosclerotic preventive and treatment strategies in clinical practice. Full article
(This article belongs to the Special Issue Molecular Studies in Aging: New Advances)
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17 pages, 3809 KiB  
Review
Molecular Mechanisms Associated with Aging Kidneys and Future Perspectives
by Min-Jee Jo, Joo-Kyung Lee, Ji-Eun Kim and Gang-Jee Ko
Int. J. Mol. Sci. 2023, 24(23), 16912; https://doi.org/10.3390/ijms242316912 - 29 Nov 2023
Cited by 1 | Viewed by 916
Abstract
The rapid growth of the elderly population is making the need for extensive and advanced information about age-related organ dysfunction a crucial research area. The kidney is one of the organs most affected by aging. Aged kidneys undergo functional decline, characterized by a [...] Read more.
The rapid growth of the elderly population is making the need for extensive and advanced information about age-related organ dysfunction a crucial research area. The kidney is one of the organs most affected by aging. Aged kidneys undergo functional decline, characterized by a reduction in kidney size, decreased glomerular filtration rate, alterations in renal blood flow, and increased inflammation and fibrosis. This review offers a foundation for understanding the functional and molecular mechanisms of aging kidneys and for selecting identifying appropriate targets for future treatments of age-related kidney issues. Full article
(This article belongs to the Special Issue Molecular Studies in Aging: New Advances)
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17 pages, 884 KiB  
Review
The Central Role of the NAD+ Molecule in the Development of Aging and the Prevention of Chronic Age-Related Diseases: Strategies for NAD+ Modulation
by Borut Poljšak, Vito Kovač, Stjepan Špalj and Irina Milisav
Int. J. Mol. Sci. 2023, 24(3), 2959; https://doi.org/10.3390/ijms24032959 - 03 Feb 2023
Cited by 4 | Viewed by 6549
Abstract
The molecule NAD+ is a coenzyme for enzymes catalyzing cellular redox reactions in several metabolic pathways, encompassing glycolysis, TCA cycle, and oxidative phosphorylation, and is a substrate for NAD+-dependent enzymes. In addition to a hydride and electron transfer in redox reactions, NAD+ is [...] Read more.
The molecule NAD+ is a coenzyme for enzymes catalyzing cellular redox reactions in several metabolic pathways, encompassing glycolysis, TCA cycle, and oxidative phosphorylation, and is a substrate for NAD+-dependent enzymes. In addition to a hydride and electron transfer in redox reactions, NAD+ is a substrate for sirtuins and poly(adenosine diphosphate–ribose) polymerases and even moderate decreases in its cellular concentrations modify signaling of NAD+-consuming enzymes. Age-related reduction in cellular NAD+ concentrations results in metabolic and aging-associated disorders, while the consequences of increased NAD+ production or decreased degradation seem beneficial. This article reviews the NAD+ molecule in the development of aging and the prevention of chronic age-related diseases and discusses the strategies of NAD+ modulation for healthy aging and longevity. Full article
(This article belongs to the Special Issue Molecular Studies in Aging: New Advances)
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30 pages, 916 KiB  
Review
Aging Effects on Optic Nerve Neurodegeneration
by Janet Coleman-Belin, Alon Harris, Bo Chen, Jing Zhou, Thomas Ciulla, Alice Verticchio, Gal Antman, Michael Chang and Brent Siesky
Int. J. Mol. Sci. 2023, 24(3), 2573; https://doi.org/10.3390/ijms24032573 - 29 Jan 2023
Cited by 4 | Viewed by 4096
Abstract
Common risk factors for many ocular pathologies involve non-pathologic, age-related damage to the optic nerve. Understanding the mechanisms of age-related changes can facilitate targeted treatments for ocular pathologies that arise at any point in life. In this review, we examine these age-related, neurodegenerative [...] Read more.
Common risk factors for many ocular pathologies involve non-pathologic, age-related damage to the optic nerve. Understanding the mechanisms of age-related changes can facilitate targeted treatments for ocular pathologies that arise at any point in life. In this review, we examine these age-related, neurodegenerative changes in the optic nerve, contextualize these changes from the anatomic to the molecular level, and appreciate their relationship with ocular pathophysiology. From simple structural and mechanical changes at the optic nerve head (ONH), to epigenetic and biochemical alterations of tissue and the environment, multiple age-dependent mechanisms drive extracellular matrix (ECM) remodeling, retinal ganglion cell (RGC) loss, and lowered regenerative ability of respective axons. In conjunction, aging decreases the ability of myelin to preserve maximal conductivity, even with “successfully” regenerated axons. Glial cells, however, regeneratively overcompensate and result in a microenvironment that promotes RGC axonal death. Better elucidating optic nerve neurodegeneration remains of interest, specifically investigating human ECM, RGCs, axons, oligodendrocytes, and astrocytes; clarifying the exact processes of aged ocular connective tissue alterations and their ultrastructural impacts; and developing novel technologies and pharmacotherapies that target known genetic, biochemical, matrisome, and neuroinflammatory markers. Management models should account for age-related changes when addressing glaucoma, diabetic retinopathy, and other blinding diseases. Full article
(This article belongs to the Special Issue Molecular Studies in Aging: New Advances)
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