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Regulatory mechanisms of age-related degenerative diseases: Insights from the gut microbiota-cellular senescence interaction network.

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Τίτλος: Regulatory mechanisms of age-related degenerative diseases: Insights from the gut microbiota-cellular senescence interaction network.
Συγγραφείς: Sun P; College of Physical Education and Health, East China Normal University, Shanghai 200241, PR China; The key Laboratory of Adolescent Health Assessment and Exercise Intervention of the Ministry of Education, East China Normal University, Shanghai 200241, PR China. Electronic address: psun@tyxx.ecnu.edu.cn., Chen G; College of Physical Education and Health, East China Normal University, Shanghai 200241, PR China., Guo Y; College of Physical Education and Health, East China Normal University, Shanghai 200241, PR China.
Πηγή: Ageing research reviews [Ageing Res Rev] 2026 Jul; Vol. 119, pp. 103152. Date of Electronic Publication: 2026 Apr 29.
Τύπος έκδοσης: Journal Article; Review
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Science Country of Publication: England NLM ID: 101128963 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-9649 (Electronic) Linking ISSN: 15681637 NLM ISO Abbreviation: Ageing Res Rev Subsets: MEDLINE
Imprint Name(s): Original Publication: Oxford, UK : Elsevier Science, c2002-
Ιατρικοί όροι (MeSH): Cellular Senescence*/physiology , Gastrointestinal Microbiome*/physiology , Aging*/metabolism , Aging*/pathology , Neurodegenerative Diseases*/microbiology , Neurodegenerative Diseases*/metabolism, Humans ; Animals ; Intestinal Barrier Function ; Senescence-Associated Secretory Phenotype
Περίληψη: Global population aging has sharply increased the prevalence of age-related degenerative diseases, posing severe challenges to global public health and socioeconomic stability. Growing evidence links these disorders to the bidirectional crosstalk between gut microbiota and cellular senescence, yet the integrated interaction network governing multi-organ degeneration remains poorly defined. Age-related gut microbial remodeling reshapes metabolite profiles: beneficial metabolites mitigate cellular senescence through epigenetic regulation, antioxidant defense, inflammatory signaling inhibition, intestinal barrier maintenance and immune modulation, while detrimental metabolites induce cellular senescence via inflammatory cascade activation, mitochondrial dysfunction, DNA damage, endoplasmic reticulum stress and intestinal barrier impairment. The intestinal barrier-immune axis mediates the systemic propagation of senescence signals, and senescent cells together with their senescence-associated secretory phenotype (SASP) further exacerbate gut microbial dysbiosis to form a pathological vicious cycle. This review systematically dissects this interaction network and its pathogenic role in major degenerative diseases, and highlights precision targeting of this network as a promising strategy to intervene in these intractable diseases.
(Copyright © 2026. Published by Elsevier B.V.)
Competing Interests: Declaration of Competing Interest Authors declare no conflicts of interest.
Contributed Indexing: Keywords: Age-related degenerative diseases; SASP; cellular senescence; gut microbiota; gut microbiota-derived metabolites; the gut microbiota-cellular senescence axis
Entry Date(s): Date Created: 20260501 Date Completed: 20260610 Latest Revision: 20260610
Update Code: 20260611
DOI: 10.1016/j.arr.2026.103152
PMID: 42066913
Βάση Δεδομένων: MEDLINE
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  Data: Regulatory mechanisms of age-related degenerative diseases: Insights from the gut microbiota-cellular senescence interaction network.
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  Data: <searchLink fieldCode="AU" term="%22Sun+P%22">Sun P</searchLink>; College of Physical Education and Health, East China Normal University, Shanghai 200241, PR China; The key Laboratory of Adolescent Health Assessment and Exercise Intervention of the Ministry of Education, East China Normal University, Shanghai 200241, PR China. Electronic address: psun@tyxx.ecnu.edu.cn.<br /><searchLink fieldCode="AU" term="%22Chen+G%22">Chen G</searchLink>; College of Physical Education and Health, East China Normal University, Shanghai 200241, PR China.<br /><searchLink fieldCode="AU" term="%22Guo+Y%22">Guo Y</searchLink>; College of Physical Education and Health, East China Normal University, Shanghai 200241, PR China.
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  Data: <searchLink fieldCode="JN" term="%22101128963%22">Ageing research reviews</searchLink> [Ageing Res Rev] 2026 Jul; Vol. 119, pp. 103152. <i>Date of Electronic Publication: </i>2026 Apr 29.
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  Data: Journal Article; Review
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  Data: <searchLink fieldCode="MM" term="%22Cellular+Senescence%22">Cellular Senescence*</searchLink>/<searchLink fieldCode="MM" term="%22Cellular+Senescence+physiology%22">physiology</searchLink> <br /><searchLink fieldCode="MM" term="%22Gastrointestinal+Microbiome%22">Gastrointestinal Microbiome*</searchLink>/<searchLink fieldCode="MM" term="%22Gastrointestinal+Microbiome+physiology%22">physiology</searchLink> <br /><searchLink fieldCode="MM" term="%22Aging%22">Aging*</searchLink>/<searchLink fieldCode="MM" term="%22Aging+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Aging%22">Aging*</searchLink>/<searchLink fieldCode="MM" term="%22Aging+pathology%22">pathology</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurodegenerative+Diseases%22">Neurodegenerative Diseases*</searchLink>/<searchLink fieldCode="MM" term="%22Neurodegenerative+Diseases+microbiology%22">microbiology</searchLink> <br /><searchLink fieldCode="MM" term="%22Neurodegenerative+Diseases%22">Neurodegenerative Diseases*</searchLink>/<searchLink fieldCode="MM" term="%22Neurodegenerative+Diseases+metabolism%22">metabolism</searchLink><br /><searchLink fieldCode="MH" term="%22Humans%22">Humans</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Intestinal+Barrier+Function%22">Intestinal Barrier Function</searchLink> ; <searchLink fieldCode="MH" term="%22Senescence-Associated+Secretory+Phenotype%22">Senescence-Associated Secretory Phenotype</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Global population aging has sharply increased the prevalence of age-related degenerative diseases, posing severe challenges to global public health and socioeconomic stability. Growing evidence links these disorders to the bidirectional crosstalk between gut microbiota and cellular senescence, yet the integrated interaction network governing multi-organ degeneration remains poorly defined. Age-related gut microbial remodeling reshapes metabolite profiles: beneficial metabolites mitigate cellular senescence through epigenetic regulation, antioxidant defense, inflammatory signaling inhibition, intestinal barrier maintenance and immune modulation, while detrimental metabolites induce cellular senescence via inflammatory cascade activation, mitochondrial dysfunction, DNA damage, endoplasmic reticulum stress and intestinal barrier impairment. The intestinal barrier-immune axis mediates the systemic propagation of senescence signals, and senescent cells together with their senescence-associated secretory phenotype (SASP) further exacerbate gut microbial dysbiosis to form a pathological vicious cycle. This review systematically dissects this interaction network and its pathogenic role in major degenerative diseases, and highlights precision targeting of this network as a promising strategy to intervene in these intractable diseases.<br /> (Copyright © 2026. Published by Elsevier B.V.)
– Name: Abstract
  Label: Competing Interests
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  Data: Declaration of Competing Interest Authors declare no conflicts of interest.
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  Data: <i>Keywords: </i>Age-related degenerative diseases; SASP; cellular senescence; gut microbiota; gut microbiota-derived metabolites; the gut microbiota-cellular senescence axis
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