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Autophagy Meets Aging Ⅱ
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Autophagy Meets Aging Ⅱ

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

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 12029

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

Published Papers (4 papers)

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Research

12 pages, 2496 KiB  
Article
Relationship between Mitochondrial Quality Control Markers, Lower Extremity Tissue Composition, and Physical Performance in Physically Inactive Older Adults
by Anna Picca, Matthew Triolo, Stephanie E. Wohlgemuth, Matthew S. Martenson, Robert T. Mankowski, Stephen D. Anton, Emanuele Marzetti, Christiaan Leeuwenburgh and David A. Hood
Cells 2023, 12(1), 183; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12010183 - 02 Jan 2023
Cited by 7 | Viewed by 2336
Abstract
Altered mitochondrial quality and function in muscle may be involved in age-related physical function decline. The role played by the autophagy–lysosome system, a major component of mitochondrial quality control (MQC), is incompletely understood. This study was undertaken to obtain initial indications on the [...] Read more.
Altered mitochondrial quality and function in muscle may be involved in age-related physical function decline. The role played by the autophagy–lysosome system, a major component of mitochondrial quality control (MQC), is incompletely understood. This study was undertaken to obtain initial indications on the relationship between autophagy, mitophagy, and lysosomal markers in muscle and measures of physical performance and lower extremity tissue composition in young and older adults. Twenty-three participants were enrolled, nine young (mean age: 24.3 ± 4.3 years) and 14 older adults (mean age: 77.9 ± 6.3 years). Lower extremity tissue composition was quantified volumetrically by magnetic resonance imaging and a tissue composition index was calculated as the ratio between muscle and intermuscular adipose tissue volume. Physical performance in older participants was assessed via the Short Physical Performance Battery (SPPB). Protein levels of the autophagy marker p62, the mitophagy mediator BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), the lysosomal markers transcription factor EB, vacuolar-type ATPase, and lysosomal-associated membrane protein 1 were measured by Western immunoblotting in vastus lateralis muscle biopsies. Older adults had smaller muscle volume and lower tissue composition index than young participants. The protein content of p62 and BNIP3 was higher in older adults. A negative correlation was detected between p62 and BNIP3 and the tissue composition index. p62 and BNIP3 were also related to the performance on the 5-time sit-to-stand test of the SPPB. Our results suggest that an altered expression of markers of the autophagy/mitophagy–lysosomal system is related to deterioration of lower extremity tissue composition and muscle dysfunction. Additional studies are needed to clarify the role of defective MQC in human muscle aging and identify novel biological targets for drug development. Full article
(This article belongs to the Special Issue Autophagy Meets Aging Ⅱ)
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24 pages, 14718 KiB  
Article
Follicle-Stimulating Hormone Alleviates Ovarian Aging by Modulating Mitophagy- and Glycophagy-Based Energy Metabolism in Hens
by Juan Dong, Changquan Guo, Zhaoyu Yang, Yangyang Wu and Caiqiao Zhang
Cells 2022, 11(20), 3270; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11203270 - 18 Oct 2022
Cited by 10 | Viewed by 2615
Abstract
As a predominant hormone in the reproductive axis, follicle-stimulating hormone (FSH) is known as the primary surviving factor for follicular growth. In this study, the alleviating effect of FSH on aging chicken granulosa cells (GCs) was investigated. Results showed that FSH activated mitophagy [...] Read more.
As a predominant hormone in the reproductive axis, follicle-stimulating hormone (FSH) is known as the primary surviving factor for follicular growth. In this study, the alleviating effect of FSH on aging chicken granulosa cells (GCs) was investigated. Results showed that FSH activated mitophagy and relieved mitochondrial edema in D-gal-induced senescent GCs, which was evidenced by an increased number of mitophagosomes as well as increased mitochondria-light chain 3 (LC3) colocalization. Mitophagy activation was accompanied by the activation of the AMP-activated protein kinase (AMPK) signaling pathway. Furthermore, upregulated glycophagy was demonstrated by an increased interaction of starch-binding domain protein 1 (STBD1) with GABA type A receptor-associated protein-like 1 (GABARAPL1) in D-gal-induced senescent GCs. FSH treatment further promoted glycophagy, accompanied by PI3K/AKT activation. PI3K inhibitor LY294002 and AKT inhibitor GSK690693 attenuated the effect of FSH on glycophagy and glycolysis. The inhibition of FSH-mediated autophagy attenuated the protective effect of FSH on naturally aging GC proliferation and glycolysis. The simultaneous blockage of PI3K/AKT and AMPK signaling also abolished the positive effect of FSH on naturally senescent ovarian energy regulation. These data reveal that FSH prevents chicken ovarian aging by modulating glycophagy- and mitophagy-based energy metabolism through the PI3K/AKT and AMPK pathways. Full article
(This article belongs to the Special Issue Autophagy Meets Aging Ⅱ)
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23 pages, 7163 KiB  
Article
Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer’s Disease
by Sandra Espinoza, Felipe Grunenwald, Wileidy Gomez, Felipe García, Lorena Abarzúa-Catalan, Sebastián Oyarce-Pezoa, Maria Fernanda Hernandez, Bastián I. Cortés, Markus Uhrig, Daniela P. Ponce, Claudia Durán-Aniotz, Claudio Hetz, Carol D. SanMartín, Victor H. Cornejo, Fernando Ezquer, Valentina Parra, Maria Isabel Behrens, Patricio A. Manque, Diego Rojas-Rivera, René L. Vidal, Ute Woehlbier and Melissa Nassifadd Show full author list remove Hide full author list
Cells 2022, 11(12), 1860; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11121860 - 07 Jun 2022
Cited by 3 | Viewed by 3684
Abstract
Alzheimer’s disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways [...] Read more.
Alzheimer’s disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways depending on cell type, and little information is currently available on neuronal Rubicon’s role in the AD context. Here, we investigated the cell-specific expression of Rubicon in postmortem brain samples from AD patients and 5xFAD mice and its impact on amyloid β burden in vivo and neuroblastoma cells. Further, we assessed Rubicon levels in human-induced pluripotent stem cells (hiPSCs), derived from early-to-moderate AD and in postmortem samples from severe AD patients. We found increased Rubicon levels in AD-hiPSCs and postmortem samples and a notable Rubicon localization in neurons. In AD transgenic mice lacking Rubicon, we observed intensified amyloid β burden in the hippocampus and decreased Pacer and p62 levels. In APP-expressing neuroblastoma cells, increased APP/amyloid β secretion in the medium was found when Rubicon was absent, which was not observed in cells depleted of Atg5, essential for autophagy, or Rab27a, required for exosome secretion. Our results propose an uncharacterized role of Rubicon on APP/amyloid β homeostasis, in which neuronal Rubicon is a repressor of APP/amyloid β secretion, defining a new way to target AD and other similar diseases therapeutically. Full article
(This article belongs to the Special Issue Autophagy Meets Aging Ⅱ)
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22 pages, 9076 KiB  
Article
MG132 Induces Progerin Clearance and Improves Disease Phenotypes in HGPS-like Patients’ Cells
by Karim Harhouri, Pierre Cau, Frank Casey, Koffi Mawuse Guedenon, Yassamine Doubaj, Lionel Van Maldergem, Gerardo Mejia-Baltodano, Catherine Bartoli, Annachiara De Sandre-Giovannoli and Nicolas Lévy
Cells 2022, 11(4), 610; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11040610 - 10 Feb 2022
Cited by 3 | Viewed by 2800
Abstract
Progeroid syndromes (PS), including Hutchinson-Gilford Progeria Syndrome (HGPS), are premature and accelerated aging diseases, characterized by clinical features mimicking physiological aging. Most classical HGPS patients carry a de novo point mutation within exon 11 of the LMNA gene encoding A-type lamins. This mutation [...] Read more.
Progeroid syndromes (PS), including Hutchinson-Gilford Progeria Syndrome (HGPS), are premature and accelerated aging diseases, characterized by clinical features mimicking physiological aging. Most classical HGPS patients carry a de novo point mutation within exon 11 of the LMNA gene encoding A-type lamins. This mutation activates a cryptic splice site, leading to the production of a truncated prelamin A, called prelamin A ∆50 or progerin, that accumulates in HGPS cell nuclei and is a hallmark of the disease. Some patients with PS carry other LMNA mutations and are named “HGPS-like” patients. They produce progerin and/or other truncated prelamin A isoforms (∆35 and ∆90). We previously found that MG132, a proteasome inhibitor, induced progerin clearance in classical HGPS through autophagy activation and splicing regulation. Here, we show that MG132 induces aberrant prelamin A clearance and improves cellular phenotypes in HGPS-like patients’ cells other than those previously described in classical HGPS. These results provide preclinical proof of principle for the use of a promising class of molecules toward a potential therapy for children with HGPS-like or classical HGPS. Full article
(This article belongs to the Special Issue Autophagy Meets Aging Ⅱ)
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