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8.3
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Journals
Biomolecules
Special Issues
Mechanisms and Novel Biomarkers Underlying Aging and Longevity
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Mechanisms and Novel Biomarkers Underlying Aging and Longevity

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 2653

Special Issue Editors

Dr. Ines Sanchez-Roman

E-Mail Website
Guest Editor
Department of Genetics, Physiology and Microbiology, Faculty of Biological Sciences. Complutense University of Madrid, Madrid, Spain
Interests: aging; oxidative stress; DNA maintenance; mitochondria; centenarians; premature aging
Dr. Tinna V. Stevnsner

E-Mail Website
Guest Editor
Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark Danish Aging Research Center, Aarhus, Denmark
Interests: aging; neurodegeneration; oxidative stress; mitochondria; premature aging; longevity

Special Issue Information

Dear Colleagues,

Aging is a complex biological process associated with a progressive time dependent decline in organismal function. This deterioration is the primary driver of the dominant age-associated human diseases, such as cardiovascular disorders, cancer, and neurodegeneration. These are particularly relevant due to their great influence on health-span and quality of life. Nowadays, the rapid increase in the aged population entails major health and socioeconomic problems, which challenge our society. Therefore, increasing our knowledge of the mechanisms underlying aging, as well as identification of reliable biomarkers of aging, will have a global impact. In the recent years, major progress has been made within the field of aging research, and this has resulted in the formulation of an increasing number of hallmarks of aging. Extensive studies of the various hallmarks and how they interconnect and contribute to the regulation of aging are ongoing. As aging is a complex process, modern technologies, such as deep learning techniques, as well as -omic disciplines, may have the potential to moderate this complexity in the future. The obtained new knowledge about the most relevant factors that influence the rate of aging and age-associated diseases will help to identify targets for interventions and qualify strategies to extend health-span and longevity.

We encourage scientists to send original research articles and reviews that will cover the molecular, cellular, and systemic mechanisms underpinning aging both in laboratory organisms and in human medicine. Interventions that target longevity and health-span will also be an area of great interest.

Dr. Ines Sanchez-Roman
Dr. Tinna V. Stevnsner
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. Biomolecules 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 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.

Keywords

  • aging
  • genomic instability
  • mitochondrial dysfunction
  • oxidative stress
  • premature aging
  • longevity
  • aging-associated diseases
  • interventions

Published Papers (2 papers)

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Research

15 pages, 1811 KiB  
Article
Physical Interventions Restore Physical Frailty and the Expression of CXCL-10 and IL-1β Inflammatory Biomarkers in Old Individuals and Mice
by Diego Marcos-Pérez, Sara Cruces-Salguero, Esther García-Domínguez, Marcos J. Araúzo-Bravo, Mari Carmen Gómez-Cabrera, José Viña, Itziar Vergara and Ander Matheu
Biomolecules 2024, 14(2), 166; https://0-doi-org.brum.beds.ac.uk/10.3390/biom14020166 - 31 Jan 2024
Cited by 1 | Viewed by 934
Abstract
Background: Frailty is a geriatric syndrome associated with negative health outcomes that represents a dynamic condition with a potential of reversibility after physical exercise interventions. Typically, inflammatory and senescence markers are increased in frail individuals. However, the impact that physical exercise exerts on [...] Read more.
Background: Frailty is a geriatric syndrome associated with negative health outcomes that represents a dynamic condition with a potential of reversibility after physical exercise interventions. Typically, inflammatory and senescence markers are increased in frail individuals. However, the impact that physical exercise exerts on inflammatory and senescence biomarkers remains unknown. We assessed the effect of physical intervention in old individuals and mice and determined the expression of inflammatory and senescence markers. Methods: Twelve elderly individuals were enrolled from a primary care setting to a 3-month intervention. Frailty was measured by SPPB and the expression of biomarkers by cytokine array and RT-qPCR. In addition, 12 aged C57BL/6 mice completed an intervention, and inflammation and senescence markers were studied. Results: The physical intervention improved the SPPB score, reducing frail and pre-frail individuals. This was correlated with a reduction in several pro-inflammatory biomarkers such as IL-6, CXCL-1, CXCL-10, IL-1β, IL-7, GM-CSF as well as p16INK4a and p21CIP1 senescence markers. Otherwise, the levels of anti-inflammatory biomarker IL-4 were significantly increased. Moreover, the physical intervention in mice also improved their functional capacity and restored the expression of inflammatory (Il-1β, Cxcl-10, Il-6, and Cxcl-1) and senescence (p21Cip1) markers. Additionally, PLSDA and ROC curve analysis revealed CXCL-10 and IL-1β to be the biomarkers of functional improvement in both cohorts. Conclusions: Our results showed that a physical intervention improves physical frailty, and reverses inflammation and senescence biomarkers comprising CXCL-10 and IL-1β. Full article
(This article belongs to the Special Issue Mechanisms and Novel Biomarkers Underlying Aging and Longevity)
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16 pages, 2437 KiB  
Article
Supplementing L-Citrulline Can Extend Lifespan in C. elegans and Attenuate the Development of Aging-Related Impairments of Glucose Tolerance and Intestinal Barrier in Mice
by Dragana Rajcic, Franziska Kromm, Angélica Hernández-Arriaga, Annette Brandt, Anja Baumann, Raphaela Staltner, Amélia Camarinha-Silva and Ina Bergheim
Biomolecules 2023, 13(11), 1579; https://0-doi-org.brum.beds.ac.uk/10.3390/biom13111579 - 26 Oct 2023
Viewed by 1390
Abstract
L-Citrulline (L-Cit) is discussed to possess a protective effect on intestinal barrier dysfunction but also to diminish aging-associated degenerative processes. Here, the effects of L-Cit on lifespan were assessed in C. elegans, while the effects of L-Cit on aging-associated decline were determined [...] Read more.
L-Citrulline (L-Cit) is discussed to possess a protective effect on intestinal barrier dysfunction but also to diminish aging-associated degenerative processes. Here, the effects of L-Cit on lifespan were assessed in C. elegans, while the effects of L-Cit on aging-associated decline were determined in C57BL/6J mice. For lifespan analysis, C. elegans were treated with ±5 mM L-Cit. Twelve-month-old male C57BL/6J mice (n = 8–10/group) fed a standard chow diet received drinking water ± 2.5 g/kg/d L-Cit or 5 g/kg/d hydrolyzed soy protein (Iso-N-control) for 16 or 32 weeks. Additionally, 4-month-old C57BL/6J mice were treated accordingly for 8 weeks. Markers of senescence, glucose tolerance, intestinal barrier function, and intestinal microbiota composition were analyzed in mice. L-Cit treatment significantly extended the lifespan of C. elegans. The significant increase in markers of senescence and signs of impaired glucose tolerance found in 16- and 20-month-old control mice was attenuated in L-Cit-fed mice, which was associated with protection from intestinal barrier dysfunction and a decrease in NO2− levels in the small intestine, while no marked differences in intestinal microbiota composition were found when comparing age-matched groups. Our results suggest that pharmacological doses of L-Cit may have beneficial effects on lifespan in C. elegans and aging-associated decline in mice. Full article
(This article belongs to the Special Issue Mechanisms and Novel Biomarkers Underlying Aging and Longevity)
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