Shortened Telomere Length as a Risk Factor for Idiopathic Pulmonary Fibrosis: A Meta-Analysis

Idiopathic Pulmonary Fibrosis (IPF) is a progressive lung disease with limited life expectancy after diagnosis. The median survival time ranges from 2 to 4 years, indicating a poor prognosis. Multiple telomere-related genes that cause telomere shortening have been associated with a significant percentage of IPF cases. This review aims to analyze the association of short telomere length with IPF incidence.

A systematic online search was conducted on PubMed, Scopus, and Cochrane. Articles that met the criteria were included. Quality of included literature was assessed using the Newcastle–Ottawa Scale (NOS). The pooled standard mean difference (SMD) with 95% confidence interval (CI) of telomere length was calculated using a random-effect model.

Six original studies containing 622 IPF patients and 544 controls were included in the meta-analysis. The study designs were case control and cohort. Pooled analysis showed shorter telomere length in IPF patients compared to controls (SMD: -0.84, 95%CI -1.21 to -0.48, Z = 4.55, p < 0.00001). Subgroup analysis showed that steeper telomere shortening was found in lung tissue compared to peripheral blood sample. The findings suggested that telomere length may be closely associated with the pathogenesis of pulmonary fibrosis.

Repeated cell divisions gradually shorten telomeres that lead to senescence and apoptosis. Premature senescence disrupts the balance of lung epithelial cells, potentially activating lung remodeling processes that result in fibrotic damage through senescence-associated secretory phenotype (SASP).

This study shows significant shorter telomere lengths in IPF patients compared to healthy controls that suggest telomere as a risk factor for IPF occurrence. These findings highlight the value of telomere assessment not only for early detection but also as a potential predictive biomarker for clinical outcomes.