From stress to sight: The role of mechanical forces in the retinal diseases
The retina, a light-sensitive neural tissue critical for vision, exists in a dynamic mechanical environment where it is continuously exposed to mechanical forces. These forces, including traction forces, intraocular pressure-related stress, and hemodynamic forces, are closely linked to the progressi...
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Published in | Advances in ophthalmology practice and research Vol. 5; no. 3; pp. 157 - 164 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.08.2025
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | The retina, a light-sensitive neural tissue critical for vision, exists in a dynamic mechanical environment where it is continuously exposed to mechanical forces. These forces, including traction forces, intraocular pressure-related stress, and hemodynamic forces, are closely linked to the progression of retinal diseases. A comprehensive understanding of retinal mechanosensation and mechanotransduction is essential for understanding the pathological mechanisms under aberrant mechanical conditions.
This review synthesizes current knowledge on advanced biomechanical assessment techniques, and aging-associated biomechanical alterations in retinal tissues, emphasizing how mechanical forces drive structural and functional pathology.
By elucidating the mechanosensitive mechanisms remodeling retinal cell behavior and fate, this review highlights the critical role of biomechanics in retinal disease pathogenesis. The integration of mechanistic insights with biomechanical assessment techniques offers transformative potential for diagnosing mechanical dysfunction and developing mechanotargeted therapies.
•Synthesizes current knowledge on advanced biomechanical assessment techniques, and aging-associated biomechanical alterations in retinal tissues.•Emphasizing how mechanical forces drive structural and functional pathology. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 These authors contributed equally. |
ISSN: | 2667-3762 2667-3762 |
DOI: | 10.1016/j.aopr.2025.04.002 |