Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.9
5.1
Journals
Cells
Special Issues
Autophagy Meets Aging 2025
share announcement

Autophagy Meets Aging 2025

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

Deadline for manuscript submissions: 10 June 2025 | Viewed by 9914

Special Issue Editors

Prof. Dr. Christiaan Leeuwenburgh

E-Mail Website
Guest Editor
Institute on Aging, UF Claude D. Pepper Older American Independence Center, College of Medicine, University of Florida, Gainesville, FL 32611, USA
Interests: metabolism; autophagy; mitochondria; genome instability; inflammation and aging
Special Issues, Collections and Topics in MDPI journals
Dr. Anna Picca

E-Mail Website
Guest Editor
1. Department of Medicine and Surgery, Lum Jean Monnet University, 70010 Casamassima, Italy
2. Department of Geriatrics, Neuroscience and Orthopedics, Fondazione Policlinico Universitario "A. Gemelli", IRCCS, 00168 Rome, Italy
Interests: autophagy; biogerontology; biomarkers; exosomes; inflamm-aging; metabolic markers; mitochondria; mitochondrial DNA; mitophagy; mitochondrial damage
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is marked by multiple biological disarrangements that predispose older individuals to increased vulnerability to the development of chronic diseases (e.g., cancer, diabetes, cardiovascular disease, neurodegeneration) and functional decline.

Declines in autophagy and cellular quality control systems are advocated as being among pillars of the aging process by contributing to the accrual of intracellular “waste” (e.g., protein aggregates, damaged mitochondria, and lipofuscin). Organelle-specific forms of autophagy (including mitophagy, which selectively targets mitochondria) have been identified. Due to the pro-inflammatory nature of some intracellular components, the coordinated activity of these recycling machineries is especially relevant for limiting inflamm-aging through efficient housekeeping.

This Special Issue aims to gather contributions on age-related changes in autophagy and other cellular quality control processes from different, yet complementary, points of view, by convening clinicians and basic researchers working in the field of biogerontology in humans and pre-clinical models. If the molecular determinants of these changes were to be unveiled, innovative anti-aging remedies and personalized interventions targeting cellular quality control could be developed for extending both health- and lifespan.

We therefore invite you to submit your latest original research or review articles to this Special Issue.

Prof. Dr. Christiaan Leeuwenburgh
Dr. Anna Picca
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.

Keywords

  • aging
  • autophagy
  • cellular quality control
  • mitochondrial dysfunction
  • redox biology
  • extracellular vesicles trafficking
  • inflammation
  • biomarkers
  • omics
  • behavioral and pharmacological interventions

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

22 pages, 1371 KiB  
Review
Iron Metabolism and Muscle Aging: Where Ferritinophagy Meets Mitochondrial Quality Control
by Rosa Di Lorenzo, Emanuele Marzetti, Helio José Coelho-Junior, Riccardo Calvani, Vito Pesce, Francesco Landi, Christiaan Leeuwenburgh and Anna Picca
Cells 2025, 14(9), 672; https://doi.org/10.3390/cells14090672 - 3 May 2025
Viewed by 441
Abstract
In older adults with reduced physical performance, an increase in the labile iron pool within skeletal muscle is observed. This accumulation is associated with an altered expression of mitochondrial quality control (MQC) markers and increased mitochondrial DNA damage, supporting the hypothesis that impaired [...] Read more.
In older adults with reduced physical performance, an increase in the labile iron pool within skeletal muscle is observed. This accumulation is associated with an altered expression of mitochondrial quality control (MQC) markers and increased mitochondrial DNA damage, supporting the hypothesis that impaired MQC contributes to muscle dysfunction during aging. The autophagy–lysosome system plays a critical role in MQC by tagging and engulfing proteins and organelles for degradation in lysosomes. The endolysosomal system is also instrumental in transferrin recycling, which, in turn, regulates cellular iron uptake. In the neuromuscular system, the autophagy–lysosome system supports the structural integrity of neuromuscular junctions, and its dysfunction contributes to muscle atrophy. While MQC was thought to protect against iron-induced cell death, the discovery of ferroptosis, a form of iron-dependent cell death, has highlighted a complex interplay between MQC and iron-inflicted damage. Ferritinophagy, the autophagic degradation of ferritin, if overactivated, can induce ferroptosis. Alternatively, aging may impair ferritinophagy, leading to ferritin accumulation and the release of toxic labile iron under stress, exacerbating oxidative damage and cellular senescence. Physical activity supports muscle health also by preserving mitochondrial quantity and quality and enhancing bioenergetics. However, therapeutic strategies for preventing or reversing physical function decline in aging are still lacking due to the insufficient understanding of the underlying mechanisms. Unveiling how disruptions in iron homeostasis impact muscle quality in older adults may allow for the development of therapeutic strategies targeting iron handling to alleviate age-associated muscle decline. Full article
(This article belongs to the Special Issue Autophagy Meets Aging 2025)
►▼ Show Figures

Figure 1

23 pages, 2499 KiB  
Review
Natural Autophagy Activators to Fight Age-Related Diseases
by Vianey M. Mundo Rivera, José Roberto Tlacuahuac Juárez, Nadia Mireya Murillo Melo, Norberto Leyva Garcia, Jonathan J. Magaña, Joaquín Cordero Martínez and Guadalupe Elizabeth Jiménez Gutierrez
Cells 2024, 13(19), 1611; https://doi.org/10.3390/cells13191611 - 26 Sep 2024
Cited by 3 | Viewed by 3389
Abstract
The constant increase in the elderly population presents significant challenges in addressing new social, economic, and health problems concerning this population. With respect to health, aging is a primary risk factor for age-related diseases, which are driven by interconnected molecular hallmarks that influence [...] Read more.
The constant increase in the elderly population presents significant challenges in addressing new social, economic, and health problems concerning this population. With respect to health, aging is a primary risk factor for age-related diseases, which are driven by interconnected molecular hallmarks that influence the development of these diseases. One of the main mechanisms that has attracted more attention to aging is autophagy, a catabolic process that removes and recycles damaged or dysfunctional cell components to preserve cell viability. The autophagy process can be induced or deregulated in response to a wide range of internal or external stimuli, such as starvation, oxidative stress, hypoxia, damaged organelles, infectious pathogens, and aging. Natural compounds that promote the stimulation of autophagy regulatory pathways, such as mTOR, FoxO1/3, AMPK, and Sirt1, lead to increased levels of essential proteins such as Beclin-1 and LC3, as well as a decrease in p62. These changes indicate the activation of autophagic flux, which is known to be decreased in cardiovascular diseases, neurodegeneration, and cataracts. The regulated administration of natural compounds offers an adjuvant therapeutic alternative in age-related diseases; however, more experimental evidence is needed to support and confirm these health benefits. Hence, this review aims to highlight the potential benefits of natural compounds in regulating autophagy pathways as an alternative approach to combating age-related diseases. Full article
(This article belongs to the Special Issue Autophagy Meets Aging 2025)
►▼ Show Figures

Figure 1

16 pages, 2568 KiB  
Review
Molecular Mechanisms of Autophagy Decline during Aging
by Shaun H. Y. Lim, Malene Hansen and Caroline Kumsta
Cells 2024, 13(16), 1364; https://doi.org/10.3390/cells13161364 - 16 Aug 2024
Cited by 5 | Viewed by 4638
Abstract
Macroautophagy (hereafter autophagy) is a cellular recycling process that degrades cytoplasmic components, such as protein aggregates and mitochondria, and is associated with longevity and health in multiple organisms. While mounting evidence supports that autophagy declines with age, the underlying molecular mechanisms remain unclear. [...] Read more.
Macroautophagy (hereafter autophagy) is a cellular recycling process that degrades cytoplasmic components, such as protein aggregates and mitochondria, and is associated with longevity and health in multiple organisms. While mounting evidence supports that autophagy declines with age, the underlying molecular mechanisms remain unclear. Since autophagy is a complex, multistep process, orchestrated by more than 40 autophagy-related proteins with tissue-specific expression patterns and context-dependent regulation, it is challenging to determine how autophagy fails with age. In this review, we describe the individual steps of the autophagy process and summarize the age-dependent molecular changes reported to occur in specific steps of the pathway that could impact autophagy. Moreover, we describe how genetic manipulations of autophagy-related genes can affect lifespan and healthspan through studies in model organisms and age-related disease models. Understanding the age-related changes in each step of the autophagy process may prove useful in developing approaches to prevent autophagy decline and help combat a number of age-related diseases with dysregulated autophagy. Full article
(This article belongs to the Special Issue Autophagy Meets Aging 2025)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop