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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
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Telomeres in Interstitial Lung Disease.

Carmel J W Stock1, Elisabetta A Renzoni1

  • 1Interstitial Lung Disease Unit, Royal Brompton and Harefield Clinical Group, Guy's and St Thomas' NHS Foundation Trust/National Heart and Lung Institute, Imperial College London, Sydney Street, London SW3 6NP, UK.

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|April 3, 2021
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Summary

Genetic mutations in telomere-related genes and shorter telomere length are linked to the development and progression of fibrotic interstitial lung diseases (ILD), impacting patient outcomes and treatment.

Keywords:
ILDIPFgeneticstelomerasetelomere related genestelomeres

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Area of Science:

  • Genetics and Molecular Biology
  • Pulmonary Medicine
  • Cellular Aging

Background:

  • Interstitial lung diseases (ILD) involve lung inflammation and fibrosis.
  • Telomeres protect chromosome ends, shortening with cell division and age.
  • Telomerase counteracts telomere shortening but can be affected by genetic mutations.

Purpose of the Study:

  • To review evidence linking telomere length and genetic variations to fibrotic ILDs.
  • To explore the role of telomere biology in ILD development, progression, and treatment.

Main Methods:

  • Review of recent scientific literature on telomere length and genetic variations in fibrotic ILDs.
  • Analysis of studies investigating telomere-related gene mutations (e.g., TERT, TERC) and single nucleotide polymorphisms.
  • Examination of correlations between telomere length, disease progression, survival, and treatment side effects.

Main Results:

  • Genetic mutations in telomerase components (TERT, TERC) are found in some fibrotic ILDs, leading to extremely short telomeres.
  • Shorter telomere length is associated with more rapid disease progression and worse survival in idiopathic pulmonary fibrosis (IPF) and fibrotic hypersensitivity pneumonitis (HP).
  • Short telomeres increase susceptibility to side effects from immunosuppressant drugs in IPF and fibrotic HP patients.

Conclusions:

  • Telomere dysfunction, through genetic variations or acquired shortening, plays a significant role in the pathogenesis of fibrotic ILDs.
  • Telomere length serves as a prognostic biomarker and may influence treatment strategies in fibrotic ILDs.
  • Further research into telomere biology could reveal novel therapeutic targets for ILDs.