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

Autor: Parekh M; Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA., Adhikari Y; Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA., Deshpande N; Schepens Eye Research Institute, Massachusetts Eye and Ear, Boston, MA, USA; Department of Ophthalmology, Harvard Medical School, Boston, MA, USA., Miller P; Center 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., Sperling AS; Harvard 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., Tesfaigzi Y; Harvard Medical School, Boston, MA, USA; Pulmonary and Critical Care Medicine Brigham and Women's Hospital, Boston, MA, USA., Jurkunas UV; Schepens 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.
Jazyk: angličtina
Zdroj: Experimental eye research [Exp Eye Res] 2024 Nov; Vol. 248, pp. 110089. Date of Electronic Publication: 2024 Sep 10.
DOI: 10.1016/j.exer.2024.110089
Abstrakt: 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.
Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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