# Telomere Shortening in Interstitial Lung Disease: Challenges and Promises

## TL;DR

Telomere shortening is linked to interstitial lung disease, affecting diagnosis, treatment, and prognosis, with potential for gene therapy.

## Contribution

The paper reviews recent progress on telomere shortening's role in ILD and its therapeutic implications.

## Key findings

- Telomere shortening is associated with various types of ILD and patient prognosis.
- Telomerase gene mutations reduce activity, leading to telomere shortening and disease progression.
- Gene therapy targeting telomerase shows promise for treating ILD.

## Abstract

Interstitial lung disease (ILD) is a group of diseases involving diffuse pulmonary parenchymal lesions and alveolar inflammation and interstitial fibrosis. Telomeres are repetitive DNA sequences at the end of chromosomes to maintain structural integrity and telomerase can prevent telomere shortening. Telomerase abnormalities such as related gene mutations lead to decrease in telomerase activity and telomere shortening. It has been proven that telomere shortening and telomerase abnormalities are related to the occurrence and development of ILD. Telomere shortening occurs in different types of ILD patients and is associated with prognosis. Gene therapy targeting telomerase exhibits therapeutic potential. The paper elaborates on the progress of telomere shortening in the diagnosis, differential diagnosis, treatment, and prognosis of ILD in recent years, in order to demonstrate its potential and promises and to be helpful for clinical diagnosis and treatment.

Telomerase abnormalities such as related gene mutations lead to decrease in telomerase activity and telomere shortening. Individual cells undergoing continuous division exhibit telomere shortening. A successive shortening of the telomere results in dysfunctional telomeres. This induces replicative senescence of alveolar epithelial cells and ultimately progress to pulmonary fibrosis.