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Current Research on Autophagy in Aging and Age Related Diseases

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

Deadline for manuscript submissions: 20 November 2026 | Viewed by 2014

Editor


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Guest Editor
Department of Genetics, ELTE Eötvös Loránd University, 1117 Budapest, Hungary
Interests: Caenorhabditis elegans; autophagy; aging; molecular biological techniques; gene function analysis; longevity; apoptosis; signaling mechanisms

Special Issue Information

Dear Colleagues,  

Aging is one of the greatest biological challenges with far-reaching social and economic consequences. As life expectancy increases, so does the prevalence of age-related diseases such as cancer, Alzheimer's disease, cardiovascular disorders, and diabetes. Understanding the molecular mechanisms of aging paves the way for targeted therapies and strategies to extend healthspan. 

Aging results from a complex interplay of molecular processes, including DNA damage, epigenetic modifications, telomere attrition, and cumulative cellular stress. Among the key protective mechanisms, autophagy plays a critical role in maintaining cellular homeostasis by eliminating defective mitochondria, misfolded proteins, and toxic aggregates. This tightly regulated self-degradative process enhances stress resistance and supports longevity, whereas its dysregulation accelerates aging and contributes to disease. 

In this Special Issue of IJMS we focus on recent advances in understanding the role of autophagy in aging and its impact on age-related diseases. Suitable topics include, but are not limited to, contributions that explore underlying mechanisms, potential therapeutic interventions, and broader implications for promoting longevity and healthy aging.  

Dr. Tímea Sigmond
Guest Editor

Manuscript Submission Information

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Keywords

  • autophagy
  • aging
  • molecular mechanisms
  • age related diseases
  • mitochondria

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Published Papers (2 papers)

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Review

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17 pages, 1097 KB  
Review
Autophagy: A Double-Edged Sword in the Aging of C. elegans
by Tímea Sigmond and János Barna
Int. J. Mol. Sci. 2026, 27(8), 3488; https://doi.org/10.3390/ijms27083488 - 14 Apr 2026
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Abstract
Autophagy is a tightly regulated catabolic process essential for cellular homeostasis, stress adaptation, and regeneration. In the nematode Caenorhabditis elegans, with its short lifespan, transparent body, and well-defined genetics, the process can be investigated in a tissue- and age-specific manner, making it [...] Read more.
Autophagy is a tightly regulated catabolic process essential for cellular homeostasis, stress adaptation, and regeneration. In the nematode Caenorhabditis elegans, with its short lifespan, transparent body, and well-defined genetics, the process can be investigated in a tissue- and age-specific manner, making it an excellent model to study the connection between autophagy and longevity. While autophagy is generally protective—promoting cellular maintenance and longevity—its dysregulation or hyperactivation during aging can be deleterious, leading to cellular stress, tissue damage, and cell death. In this context, autophagy can act as a double-edged sword: its beneficial effects can become harmful if hyperactivated or improperly controlled, particularly in post-reproductive or stressed tissues. Here, we review studies in C. elegans that link autophagy to lifespan regulation, with a focus on unexpected, context-dependent, or harmful effects of modulating autophagy-related genes during aging. We highlight how age- and tissue-specific regulation of autophagy can optimize its protective role and discuss the implications of these findings for designing strategies to promote healthy aging, potentially providing insights for the therapeutic targeting of autophagy in humans. Full article
(This article belongs to the Special Issue Current Research on Autophagy in Aging and Age Related Diseases)
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Other

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11 pages, 3064 KB  
Brief Report
Autophagy Is Suppressed in Peripheral Blood Mononuclear Cells During Chronic Obstructive Pulmonary Disease
by James M. Cooper, Shiye Chen, Susan E. Lester, Julia Kim, Jason Gummow, Thomas Crowhurst, Emily Lawton, Arash Badiei, Phan T. Nguyen, Paul N. Reynolds, Hubertus P. A. Jersmann and Eugene Roscioli
Int. J. Mol. Sci. 2026, 27(12), 5337; https://doi.org/10.3390/ijms27125337 - 13 Jun 2026
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Abstract
Assessing autophagy may offer insights into the pathogenesis of chronic obstructive pulmonary disease (COPD). However, measuring the dynamic aspect of autophagy is challenging, and sample manipulation can cause signal fluctuations that deviate from physiological conditions. We applied an organotypic method to quantify autophagy [...] Read more.
Assessing autophagy may offer insights into the pathogenesis of chronic obstructive pulmonary disease (COPD). However, measuring the dynamic aspect of autophagy is challenging, and sample manipulation can cause signal fluctuations that deviate from physiological conditions. We applied an organotypic method to quantify autophagy in COPD, where it frequently demonstrates disease-related dysregulation. Blood from control and COPD participants was treated with or without chloroquine. Microtubule-associated protein 1 light chain 3B II (LC3B-II) abundance was quantified in peripheral blood mononuclear cells (PBMCs), and findings were validated by transmission electron microscopy. Our observations show that while basal LC3B-II abundance was similar between groups (p = 0.60), autophagic flux was significantly lower in the COPD cohort, suggesting disruption in the regulatory factors that direct autophagosome clearance (p = 0.004). This was supported by less frequent observations of autophagy-related vacuoles in the cytosol of COPD-derived PBMCs. Our findings indicate that the suppression of autophagy can be detected in the blood of individuals with COPD, which warrants further investigation into its contribution to extrapulmonary disease processes. Full article
(This article belongs to the Special Issue Current Research on Autophagy in Aging and Age Related Diseases)
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