Evidence map›Paper›PMID 39265717›Full record

ArticleExperimental eye research2024

Long-term persistent exposure to cigarette smoke induces AhR driven corneal endothelial dysfunction in mice.

Mohit Parekh, Yadav Adhikari, Neha Deshpande, Peter Miller, Adam S Sperling, Yohannes Tesfaigzi, Ula V Jurkunas

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental eye research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

7 authors.

Mohit ParekhSchepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA.
Yadav AdhikariSchepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA.
Neha DeshpandeSchepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA.
Peter MillerCenter for Cancer Research, Massachusetts General Hospital, Boston, MA, USA; Center for Regenerative Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Adam S SperlingHarvard Medical School, Boston, MA, USA; Broad Institute of MIT and Harvard, Cambridge, MA, USA; Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Yohannes TesfaigziHarvard Medical School, Boston, MA, USA; Pulmonary and Critical Care Medicine Brigham and Women's Hospital, Boston, MA, USA.
Ula V JurkunasSchepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. Electronic address: ula_jurkunas@meei.harvard.edu.

Funding

The Role of Oxidative Stress in the Pathogenesis of Fuchs Endothelial Corneal DysR01EY020581 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Ula V. Jurkunas · 2010 to 2026
$8.0M
NEI NIH HHS R01 EY020581
6 · The paper itself

Abstract

Epidemiological studies show cigarette smoking enhances corneal endothelial dysfunction, but mechanisms remain unclear. Our study reveals that prolonged smoke exposure activates the aryl hydrocarbon receptor (AhR), increasing CYP1B1 expression and accelerating senescence and fibrosis in corneal endothelium, potentially reflecting adaptive responses to maintain corneal resilience. Although these molecular modifications indicate early endothelial dysfunction, no pathological changes were observed. The findings indicate that while chronic cigarette smoke exposure triggers initial molecular alterations and endothelial dysfunction, the progression to Fuchs endothelial corneal dystrophy likely requires additional environmental or genetic factors beyond smoke exposure alone.

Indexed as

Cytochrome P-450 CYP1B1Endothelium, CornealReceptors, Aryl HydrocarbonAnimalsBasic Helix-Loop-Helix ProteinsCigarette SmokingDisease Models, AnimalFemaleFuchs' Endothelial DystrophyMaleMiceMice, Inbred C57BLBasic Helix-Loop-Helix ProteinsCyp1b1 protein, mouseCytochrome P-450 CYP1B1Receptors, Aryl HydrocarbonAryl hydrocarbon receptorCigarette smokeCorneaEndothelial dysfunctionEndothelium

Identifiers

PMID39265717
PMCPMC11531995

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Registered trials

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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.