ReviewFrontiers in medicine2021
Telomere Dysfunction in Idiopathic Pulmonary Fibrosis.
Review in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Short leukocyte telomere length across fibrotic interstitial lung disease phenotypes: An Indian pilot study.Lung India : official organ of Indian Chest Society · 2026Article
- Telomere dysfunction and mucociliary impairment drive idiopathic pulmonary fibrosis susceptibility: insights from a Sardinian whole-exome study.BMJ open respiratory research · 2026Article
- Telomere biology disorders associated with childhood interstitial lung disease.Clinical and experimental pediatrics · 2026Article
- Clinical and genetic features of idiopathic pulmonary fibrosis in a Korean cohort.Respiratory research · 2026Article
- Shortened Telomere Length as a Risk Factor for Idiopathic Pulmonary Fibrosis: A Meta-Analysis.The open respiratory medicine journal · 2026Review
- Advances in diagnosis of lung fibrosis: focus on present and future approaches.Frontiers in medicine · 2026Review
- Familial interstitial lung disease: emerging insights into screening and genetic risk.Frontiers in medicine · 2026Review
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- Age-related diseases as a testbed for anti-aging therapeutics: the case of idiopathic pulmonary fibrosis.Aging · 2025Review
- Peripheral and pulmonary telomere lengths in patients with non-idiopathic pulmonary fibrosis interstitial lung diseases.BMC pulmonary medicine · 2025Article
- Article
- Senotherapy for chronic lung disease.Pharmacological reviews · 2025Review
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Review
- The relationship between telomere length and aging-related diseases.Clinical and experimental medicine · 2025Review
- Regenerative Capacity of Alveolar Type 2 Cells Is Proportionally Reduced Following Disease Progression in Idiopathic Pulmonary Fibrosis-Derived Organoid Cultures.Tuberculosis and respiratory diseases · 2025Article
- Genetic Risk Factors in Idiopathic and Non-Idiopathic Interstitial Lung Disease: Similarities and Differences.Medicina (Kaunas, Lithuania) · 2024Review
- RIOK2 transcriptionally regulates TRiC and dyskerin complexes to prevent telomere shortening.Nature communications · 2024Article
- TNKS1BP1 mediates AECII senescence and radiation induced lung injury through suppressing EEF2 degradation.Respiratory research · 2024Article
- Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis is an age-dependent progressive and fatal lung disease of unknown etiology, which is characterized by the excessive accumulation of extracellular matrix inside the interstitial layer of the lung parenchyma that leads to abnormal scar architecture and compromised lung function capacity. Recent genetic studies have attributed the pathological genes or genetic mutations associated with familial idiopathic pulmonary fibrosis (IPF) and sporadic IPF to telomere-related components, suggesting that telomere dysfunction is an important determinant of this disease. In this study, we summarized recent advances in our understanding of how telomere dysfunction drives IPF genesis. We highlighted the key role of alveolar stem cell dysfunction caused by telomere shortening or telomere uncapping, which bridged the gap between telomere abnormalities and fibrotic lung pathology. We emphasized that senescence-associated secretory phenotypes, innate immune cell infiltration, and/or inflammation downstream of lung stem cell dysfunction influenced the native microenvironment and local cell signals, including increased transforming growth factor-beta (TGF-β) signaling in the lung, to induce pro-fibrotic conditions. In addition, the failed regeneration of new alveoli due to alveolar stem cell dysfunction might expose lung cells to elevated mechanical tension, which could activate the TGF-β signaling loop to promote the fibrotic process, especially in a periphery-to-center pattern as seen in IPF patients. Understanding the telomere-related molecular and pathophysiological mechanisms of IPF would provide new insights into IPF etiology and therapeutic strategies for this fatal disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.