> Publications > Vitamin E Alleviates Oxidative Damage and Attenuates Ferroptosis Caused by Prolonged Contraction of the Ciliary Muscle by Activating ACOT7

Photorefractor

Publication

March 26, 2026 • ✎ STRIA TECH

Vitamin E Alleviates Oxidative Damage and Attenuates Ferroptosis Caused by Prolonged Contraction of the Ciliary Muscle by Activating ACOT7

$Effects of Car treatment on refraction, AL, and PD in guinea pigs$

Topics:

Myopia

Myopia, Refractive Development and Eye Growth

Toxicity

Publication

Investigative Ophthalmology & Visual Science (Jan 05, 2026) Vitamin E Alleviates Oxidative Damage and Attenuates Ferroptosis Caused by Prolonged Contraction of the Ciliary Muscle by Activating ACOT7

Cao H, Wu J, Xiang Y, Gao X, Kou J, Cheng H, Tan Y, Wan W, Liang L, Kang J, Zheng S, Hu K

DOI: 10.1167/iovs.67.1.61 >>

The study found that prolonged contraction of the eye’s ciliary muscle damages its cells by increasing oxidative stress, disturbing iron balance, and triggering ferroptosis in guinea pigs and cultured cells. Striatech’s Photorefractor was used to track changes in refractive error over time, providing a functional measure of how well the eye could still focus. Vitamin E eye drops reduced these harmful changes and helped preserve ciliary muscle function, likely by activating the protective enzyme ACOT7.

Background: The ciliary muscle, a critical intraocular smooth muscle, plays a potent role in ocular accommodation. Investigating the potential detrimental effects on the ciliary muscle during prolonged contraction and precise mechanism underlying the cell damage hold significance in treating ciliary muscle dysfunction. The effect and mechanism of vitamin E (VitE), an antioxidant, in mitigating these adverse effects of prolonged contraction remains to be thoroughly elucidated. Methods: A guinea pig model of prolonged contraction of the ciliary muscle was established through topical administration of carbachol, and primary ciliary muscle cells isolated from guinea pigs were used for in vitro experiments. Results: The ophthalmic examination results demonstrated that prolonged contraction of the ciliary muscle impaired accommodative function in guinea pigs. This condition may lead to disrupted cellular migration, intracellular adenosine triphosphate depletion, decreased mitochondrial membrane potential, and reactive oxygen species accumulation. Further examination revealed that carbachol induced darker-stained mitochondrial membranes and diminished cristae density, consistent with morphological features of ferroptosis. Moreover, sustained cell contraction modulated specific contraction-related proteins (α-smooth muscle actin), concurrently decreased the expression of antioxidant proteins (glutathione peroxidase, superoxide dismutase, catalase, and GSH) in both tissue specimens and cells, culminating in ferroptosis in vivo and in vitro experiments. Our findings demonstrated that pretreatment with VitE alleviated oxidative injury and mitigated ferroptosis. Additionally, knocking down acetyl-coenzyme A thiosterase 7 attenuated the beneficial effect of VitE. Conclusions: These findings collectively indicated that VitE presented a viable approach to ameliorate oxidative stress and ferroptosis induced by prolonged contraction of the ciliary muscle via activating acetyl-coenzyme A thiosterase 7.