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Related Experiment Video

Updated: Feb 22, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Telomere Damage Response and Low-Grade Inflammation.

Lihui Wang1, Xianhua Yu2, Jun-Ping Liu2,3,4,5

  • 1Institute of Ageing Research, Hangzhou Normal University School of Medicine, 1378 Wenyi Road West, Hangzhou, Zhejiang Province, 311121, China. wanglihui100@163.com.

Advances in Experimental Medicine and Biology
|September 19, 2017
PubMed
Summary

Telomere attrition triggers lung inflammation and stem cell senescence. This study reveals an alternative secretory phenotype (A-SASP) involving telomere position effects and damage signals, not direct cytokine production by senescent cells.

Keywords:
CytokinesImmune cellsInflammationTelomere dysfunctionTissue senescence

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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

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Area of Science:

  • Cellular biology
  • Genomics
  • Immunology

Background:

  • Telomeres protect chromosome ends but shorten with cell division and stress.
  • Telomere attrition causes epithelial stem cell senescence and lung inflammation (SALI).
  • Mechanisms of SALI, particularly the source of secreted factors, are not fully understood.

Purpose of the Study:

  • To investigate the mechanisms underlying senescence-associated low-grade inflammation (SALI) induced by telomere attrition.
  • To identify the source of cytokines in SALI and explore alternative senescence-associated secretory phenotypes (A-SASP).

Main Methods:

  • Analysis of gene expression in senescent epithelial stem cells with telomere erosion.
  • Investigation of cytokine profiles in the cellular milieu.
  • Evaluation of telomere position effects (TPEs) and damage-associated molecular patterns (DAMPs).

Main Results:

  • Senescent epithelial stem cells with telomere erosion did not show increased cytokine gene expression.
  • Evidence suggests an alternative senescence-associated secretory phenotype (A-SASP) is involved.
  • Telomere loss leads to genomic alterations and cleaved telomeric DNA accumulation.

Conclusions:

  • Telomere position effects (TPEs) on gene expression and DAMPs in antigen presentation contribute to A-SASP and SALI.
  • Telomere damage, rather than direct cytokine production by senescent cells, drives lung inflammation.