Evidence map›Paper›PMID 35532056›Full record

ReviewPhysiological reviews2022

Telomere-mediated lung disease.

Jonathan K Alder, Mary Armanios

Open access · hybridAbstract readReview
In one paragraph

Review in Physiological reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
12.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 107 citations in OpenAlex.

  1. The Hallmarks of Aging: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 2026
    Review
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  4. Multi-omics insights into the mechanisms and prognosis of IPF.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
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13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Jonathan K AlderDivision of Pulmonary and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.ORCID 0000-0003-3741-6512
Mary ArmaniosDepartments of Oncology and Genetic Medicine, Telomere Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0002-7105-1847
Johns Hopkins University · USUniversity of Pittsburgh · US

Funding

Mechanisms of Telomere-Induced EmphysemaR01HL119476 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ARMANIOS, MARY Y · 2014 to 2023
$4.5M
Mechanisms of Telomere-Mediated Lung DiseaseR01HL135062 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jonathan K. Alder · 2018 to 2026
$4.1M
Cancer Genetics of Short Telomere SyndromesR01CA225027 · NCI · JOHNS HOPKINS UNIVERSITY · PI ARMANIOS, MARY Y · 2018 to 2022
$2.4M
NCI NIH HHS R01 CA225027NHLBI NIH HHS R01 HL119476NHLBI NIH HHS R01 HL135062
6 · The paper itself

Abstract

Parenchymal lung disease is the fourth leading cause of death in the United States; among the top causes, it continues on the rise. Telomeres and telomerase have historically been linked to cellular processes related to aging and cancer, but surprisingly, in the recent decade genetic discoveries have linked the most apparent manifestations of telomere and telomerase dysfunction in humans to the etiology of lung disease: both idiopathic pulmonary fibrosis (IPF) and emphysema. The short telomere defect is pervasive in a subset of IPF patients, and human IPF is the phenotype most intimately tied to germline defects in telomere maintenance. One-third of families with pulmonary fibrosis carry germline mutations in telomerase or other telomere maintenance genes, and one-half of patients with apparently sporadic IPF have short telomere length. Beyond explaining genetic susceptibility, short telomere length uncovers clinically relevant syndromic extrapulmonary disease, including a T-cell immunodeficiency and a propensity to myeloid malignancies. Recognition of this subset of patients who share a unifying molecular defect has provided a precision medicine paradigm wherein the telomere-mediated lung disease diagnosis provides more prognostic value than histopathology or multidisciplinary evaluation. Here, we critically evaluate this progress, emphasizing how the genetic findings put forth a new pathogenesis paradigm of age-related lung disease that links telomere abnormalities to alveolar stem senescence, remodeling, and defective gas exchange.

Indexed as

Idiopathic Pulmonary FibrosisLung DiseasesTelomeraseHumansLungTelomereTelomeraseemphysemapulmonary fibrosissenescencestem cellstelomerase

Identifiers

PMID35532056
PMCPMC9306791
OpenAlexW4229363756

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.