Therapeutic Opportunities Presented by Modulation of Cellular Senescence

Richard G.A. Faragher, Neda Heidari, Elizabeth L. Ostler

Research output: Chapter in Book/Conference proceeding with ISSN or ISBNChapterpeer-review


Cellular senescence is a permanent state of growth arrest coupled with profound changes in phenotype that can be triggered by multiple extrinsic or intrinsic stimuli. Senescence is a process-level example of the evolution of ageing mechanisms through antagonistic pleiotropy and plays a primary role in tumour suppression, although evidence is mounting for its involvement in other fundamental physiological processes. Evidence from human premature ageing diseases and from transgenic mice in which it is possible to specifically delete senescent cells is consistent with a model in which the accumulation of senescent cells through the life course is responsible for later life chronic disease and impairment. The removal of senescent cells or their reversion to a phenotypically benign state is thus an important emerging goal of translational medicine. Modern bioinformatic approaches based on text mining have compiled co-mentions of cell senescence and age-related diseases allowing an impartial ranking of the impairments most closely associated with this process. Following this schema, the evidence for the involvement of senescence in several highly ranked pathologies is reviewed, alongside potential methods for the ablation of senescent cells or their reversion to their primary phenotype with polyphenolics or inhibitors of p38 MAP kinase. Lastly, the potential for senescence to act as a barrier to the development of bioartificial organs designed to treat some of these conditions is discussed.

Original languageEnglish
Title of host publicationBiochemistry and Cell Biology of Ageing
Subtitle of host publicationPart III Biomedical Science
Number of pages19
ISBN (Electronic)9783031214103
Publication statusPublished - 5 Jan 2023

Publication series

NameSubcellular Biochemistry
ISSN (Print)0306-0225

Bibliographical note

Publisher Copyright:
© 2023, The Author(s), under exclusive license to Springer Nature Switzerland AG.


  • Ageing
  • Chondrocyte
  • Fibroblast
  • Hepatocyte
  • Kidney
  • Liver
  • p38-MAP kinase
  • Resveratrol
  • Senescence
  • Senolytic
  • Senomorphic
  • Tubular epithelial cell


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