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The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.

The connection between aging, cellular senescence and gut microbiome alterations: A comprehensive review

Jang, Dong‐Hyun, Shin, Ji‐Won, Shim, Eunha, Ohtani, Naoko, Jeon, Ok Hee·2024·Aging Cell
DOI 10.1111/acel.14315PMC PMC11464129
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Abstract

The intricate interplay between cellular senescence and alterations in the gut microbiome emerges as a pivotal axis in the aging process, increasingly recognized for its contribution to systemic inflammation, physiological decline, and predisposition to age‐associated diseases. Cellular senescence, characterized by a cessation of cell division in response to various stressors, induces morphological and functional changes within tissues. The complexity and heterogeneity of senescent cells, alongside the secretion of senescence‐associated secretory phenotype, exacerbate the aging process through pro‐inflammatory pathways and influence the microenvironment and immune system. Concurrently, aging‐associated changes in gut microbiome diversity and composition contribute to dysbiosis, further exacerbating systemic inflammation and undermining the integrity of various bodily functions. This review encapsulates the burgeoning research on the reciprocal relationship between cellular senescence and gut dysbiosis, highlighting their collective impact on age‐related musculoskeletal diseases, including osteoporosis, sarcopenia, and osteoarthritis. It also explores the potential of modulating the gut microbiome and targeting cellular senescence as innovative strategies for healthy aging and mitigating the progression of aging‐related conditions. By exploring targeted interventions, including the development of senotherapeutic drugs and probiotic therapies, this review aims to shed light on novel therapeutic avenues. These strategies leverage the connection between cellular senescence and gut microbiome alterations to advance aging research and development of interventions aimed at extending health span and improving the quality of life in the older population.

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  • Conjugated bile acids activate the farnesoid X receptor, suppressing hepatic stellate cell activation and fibrogenic signaling, thereby ameliorating liver fibrosis.

    “Additional microbial metabolites, such as conjugated bile acids, can activate the farnesoid X receptor, suppressing hepatic stellate cell activation and fibrogenic signaling, thereby ameliorating liver fibrosis105,106.”

    From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [106]

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Metadata

Authors
Jang, D., Shin, J., Shim, E., Ohtani, N., & Jeon, O. H.
Venue
Aging Cell
Publisher
Wiley
Published
2024-08-15
Volume
23
Issue
10
ISSN
  • 1474-9718
  • 1474-9726
DOI
10.1111/acel.14315
PMC
PMC11464129
Cited by
84
References
45
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Ministry of Science and ICT, South Korea (RS‐2023‐00220894)

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