Doxycycline mitigates corneal fibrosis by suppressing the focal adhesion pathway

The cornea, as a key barrier of intraocular tissues, is vulnerable to various injury factors. Acute alkali burns, as an ophthalmic emergency, can cause serious pathological changes such as persistent corneal epithelial defects, ulcers and even perforations. Doxycycline has been proven to have inhibi...

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Bibliographic Details
Published inExperimental eye research Vol. 258; p. 110506
Main Authors Zhou, Jiaxin, He, Bingbing, Zou, Wenjin
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.09.2025
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Summary:The cornea, as a key barrier of intraocular tissues, is vulnerable to various injury factors. Acute alkali burns, as an ophthalmic emergency, can cause serious pathological changes such as persistent corneal epithelial defects, ulcers and even perforations. Doxycycline has been proven to have inhibitory effects on matrix metalloproteinases and anti-inflammatory effects, etc. This study focuses on the therapeutic value of doxycycline in corneal alkali burns. In vitro experiments have shown that it can significantly inhibit the expression of Fibronectin and Collagen III by regulating the Focal adhesion(FA) signaling pathway, thereby reducing corneal scar. In vivo experiments further confirmed that doxycycline eye drops accelerated wound healing and improved corneal transparency through the FA signaling pathway. In conclusion, this study systematically clarified the corneal protection mechanism mediated by doxycycline through the FA signaling pathway, providing a new intervention strategy for the prevention and treatment of corneal alkali burns in clinical practice. •This study demonstrates the groundbreaking application of the doxycycline in treating corneal scars.•This work reveals a novel mechanism linking the focal adhesion pathway to corneal scar formation.•This study elucidated the detailed molecular mechanism through which doxycycline suppresses corneal scar formation.
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ISSN:0014-4835
1096-0007
1096-0007
DOI:10.1016/j.exer.2025.110506