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Life
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The Age of Longevity: Unpacking Biogerontology and the Future of...
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The Age of Longevity: Unpacking Biogerontology and the Future of Human Life

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: 28 August 2026 | Viewed by 1607

Special Issue Editor

Dr. Paweł Kordowitzki

E-Mail Website
Guest Editor
Department of Basic and Preclinical Sciences, Institute of Veterinary Medicine, Faculty of Biological and Veterinary Sciences, Nicolaus Copernicus University in Torun, 87-100 Torun, Poland
Interests: ageing; reproductive ageing; epigenetics clocks; DNA methylation; longevity

Special Issue Information

Dear Colleagues, 

Advances in biogerontology are rapidly redefining the boundaries of human health and lifespan, positioning society at the threshold of an unprecedented “age of longevity.” This Special Issue welcomes original and review articles about the implications of emerging interventions designed to slow, halt, or potentially reverse biological aging.

As breakthroughs in cellular senescence, stem cell dynamics, genomic stability, and systemic inflammation reshape our understanding of aging, biogerontology is shifting from descriptive science toward targeted intervention. The articles in this Special Issue will explore emerging mechanisms that drive biological aging and highlight innovative strategies—such as senolytics, gene editing, epigenetic reprogramming, and metabolic modulation—that have the potential to extend healthspan and delay age-related decline. By examining both established and cutting-edge findings, the Special Issue aims to clarify how aging operates as a coordinated, multilayered biological process and how interventions may influence the trajectory of human life. Topics related to the ethical aspects and the use of artificial intelligence in aging and biogerontology are also being explored. Together, these contributions provide a comprehensive view of the scientific landscape that is shaping the future of longevity research and its transformative implications for human life. 

Dr. Paweł Kordowitzki
Guest Editor

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 250 words) can be sent to the Editorial Office for assessment.

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. Life 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 2600 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

  • biogerontology
  • biological aging
  • longevity
  • healthspan extension
  • cellular senescence
  • epigenetic reprogramming
  • senolytics
  • gene editing
  • artificial intelligence in aging research

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Published Papers (1 paper)

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Research

14 pages, 1623 KB  
Article
FURIN Stimulates NOTCH2 and NOTCH3 Pathways, Leading to Return of Function in Aged Cells
by Peter L. Elkin, Jiaxing Liu, Jisaiah T. Wheeler, Thomas M. Suchyna and Wilma A. Hofmann
Life 2026, 16(4), 588; https://doi.org/10.3390/life16040588 - 1 Apr 2026
Viewed by 1264
Abstract
Background: Aging is accompanied by a progressive decline in skeletal muscle regeneration, largely due to impaired myogenic differentiation. The proprotein convertase FURIN is a key protease responsible for activating several signaling molecules, including precursors of NOTCH receptors, which regulate cell fate and differentiation. [...] Read more.
Background: Aging is accompanied by a progressive decline in skeletal muscle regeneration, largely due to impaired myogenic differentiation. The proprotein convertase FURIN is a key protease responsible for activating several signaling molecules, including precursors of NOTCH receptors, which regulate cell fate and differentiation. In this study, we investigated whether age-associated downregulation of FURIN contributes to impaired NOTCH2/3 signaling and myogenic function. Methods: An initial bioinformatics analysis of public scRNA-seq data from Genotype-Tissue Expression (GTEx) project indicated age-related expression of genes in the NOTCH signaling pathway. In vitro verification used early- and late-passage C2C12 myoblasts as a model of muscle cell aging to compare the expression of these genes. Late-passage C2C12 cells were transiently transfected with FURIN plasmid to assess restoration of differentiation potential, quantified by the fusion index, myogenic marker expression, and morphology. Results: Expression of FURIN, NOTCH2 and NOTCH3 was negatively correlated with age, whereas GZMB increased with age in GTEx dataset. Late-passage myoblasts exhibited impaired myotube formation, reflecting age-associated loss of myogenic capacity. Restoration of FURIN expression in aged myoblasts was associated with reduced GZMB levels, increased expression of embryonic myosin heavy chain IGF1, and partial recovery of myogenic differentiation and myotube formation. Conclusions: These findings suggest that age-associated loss of FURIN contributes to impaired NOTCH2/3 pathways and myogenic dysfunction. Overexpression of FURIN partially rescues the myogenic phenotype and increases expression of early myogenic markers in aged cells, identifying FURIN as a potential regulator of muscle regenerative capacity during aging. We suggest FURIN as a promising candidate target for further investigation into the mechanisms driving aging or age-related decline. Full article
(This article belongs to the Special Issue The Age of Longevity: Unpacking Biogerontology and the Future of Human Life)
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