Evidence map›Paper›PMID 38344410›Full record

ArticleFASEB bioAdvances2024

Club cell-specific telomere protection protein 1 (TPP1) protects against tobacco smoke-induced lung inflammation, xenobiotic metabolic dysregulation, and injurious responses.

Thivanka Muthumalage, Chiara Goracci, Irfan Rahman

Open access · goldAbstract read
In one paragraph

Article in FASEB bioAdvances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

3 authors at 1 institution in 1 country.

Thivanka MuthumalageDepartment of Environmental Medicine, School of Medicine and Dentistry University of Rochester Medical Center Rochester New York USA.ORCID https://orcid.org/0000-0003-4648-9529
Chiara GoracciDepartment of Environmental Medicine, School of Medicine and Dentistry University of Rochester Medical Center Rochester New York USA.ORCID https://orcid.org/0000-0002-1811-5573
Irfan RahmanDepartment of Environmental Medicine, School of Medicine and Dentistry University of Rochester Medical Center Rochester New York USA.ORCID https://orcid.org/0000-0003-2274-2454
University of Rochester Medical Center · US

Funding

Pulmonary toxicological evaluation and chemical interactions of menthol, mint, and tobacco flavored e-cigarette productsR00ES033835 · NIEHS · PURDUE UNIVERSITY · PI MUTHUMALAGE, THIVANKA MUDALIGE · 2023 to 2025
$747k
Pulmonary toxicological evaluation and chemical interactions of menthol, mint, and tobacco flavored e-cigarette productsK99ES033835 · NIEHS · UNIVERSITY OF ROCHESTER · PI MUTHUMALAGE, THIVANKA MUDALIGE · 2021 to 2022
$282k
NIEHS NIH HHS K99 ES033835NIEHS NIH HHS R00 ES033835
6 · The paper itself

Abstract

Inhaling xenobiotics, such as tobacco smoke is a major risk factor for pulmonary diseases, e.g., COPD/emphysema, interstitial lung disease, and pre-invasive diseases. Shelterin complex or telosome provides telomeric end protection during replication. Telomere protection protein 1 (TPP1) is one of the main six subunits of the shelterin complex supporting the telomere stability and genomic integrity. Dysfunctional telomeres and shelterin complex are associated as a disease mechanism of tobacco smoke-induced pulmonary damage and disease processes. The airway epithelium is critical to maintaining respiratory homeostasis and is implicated in lung diseases. Club cells (also known as clara cells) play an essential role in the immune response, surfactant production, and metabolism. Disrupted shelterin complex may lead to dysregulated cellular function, DNA damage, and disease progression. However, it is unknown if the conditional removal of TPP1 from Club cells can induce lung disease pathogenesis caused by tobacco smoke exposure. In this study, conditional knockout of Club-cell specific TPP1 demonstrated the instability of other shelterin protein subunits, such as TRF1, dysregulation of cell cycle checkpoint proteins, p53 and downstream targets, and dysregulation of telomeric genes. This was associated with age-dependent senescence-associated genes, increased DNA damage, and upregulated RANTES/IL13/IL33 mediated lung inflammation and injury network by cigarette smoke (CS). These phenomena are also associated with alterations in cytochrome P450 and glutathione transferases, upregulated molecular pathways promoting lung lesions, bronchial neoplasms, and adenocarcinomas. These findings suggest a pivotal role of TPP1 in maintaining lung homeostasis and injurious responses in response to CS. Thus, these data TPP1 may have therapeutic value in alleviating telomere-related chronic lung diseases.

Indexed as

ACDbasal cellsbronchogenic carcinomascigarette smokeclub cellsCOPDfibrosismainstream smokeshelterinTPP1

Identifiers

PMID38344410
PMCPMC10853660
OpenAlexW4390881295

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.