突破性研究表明，药物可预防视网膜损伤（如青光眼等病例）导致的视力丧失

发布时间：2026-03-23来源：Thailand Medical News

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: A new scientific breakthrough is offering fresh hope to millions at risk of blindness, as researchers discover a powerful compound that can protect delicate eye cells from damage. The study reveals that a molecule called Liproxstatin-1 can significantly reduce vision loss caused by retinal injury, a key factor in diseases like glaucoma..

：一项新的科学突破为数百万面临失明风险的人带来了新的希望，研究人员发现了一种强大的化合物，可以保护脆弱的眼细胞免受损伤。研究表明，一种名为Liproxstatin-1的分子能够显著减少由视网膜损伤引起的视力丧失，而视网膜损伤是青光眼等疾病的关键因素。

New compound protects retinal cells and may help prevent blindness

新化合物保护视网膜细胞，可能有助于预防失明

Understanding Vision Loss at Its Root

理解视力丧失的根本原因

Vision loss in many eye diseases occurs when retinal cells, especially retinal ganglion cells, begin to die. These cells are essential for transmitting visual information from the eye to the brain. Once lost, they cannot regenerate, making early protection critical.

许多眼病导致视力丧失的原因是视网膜细胞，尤其是视网膜神经节细胞，开始死亡。这些细胞对于将视觉信息从眼睛传递到大脑至关重要。一旦丧失，它们无法再生，因此早期保护非常关键。

One major cause of this damage is a process known as ischemia–reperfusion injury. This happens when blood supply to the eye is temporarily cut off and then restored, triggering a surge of harmful oxidative stress. This stress damages cells and activates a destructive process called ferroptosis, a form of cell death linked to iron buildup and lipid damage..

这一损伤的一个主要原因是被称为缺血-再灌注损伤的过程。当眼球的血液供应暂时中断后又恢复时，就会触发大量有害的氧化应激反应。这种应激反应会损伤细胞，并激活一种称为铁死亡的破坏性过程，这是一种与铁积累和脂质损伤相关的细胞死亡形式。

This

这

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report highlights how targeting ferroptosis could be a game changer in preventing blindness.

报告强调，针对铁死亡可能成为预防失明的改变者。

The Drug That Blocks Cell Death

阻止细胞死亡的药物

Researchers tested Liproxstatin-1, a compound known to block ferroptosis, using both animal models and lab-grown retinal cells. The results were striking. Mice treated with the compound showed significantly less damage to retinal structure. Important layers of the retina remained thicker and healthier compared to untreated subjects.

研究人员使用动物模型和实验室培养的视网膜细胞测试了已知能够阻断铁死亡的化合物Liproxstatin-1。结果令人震惊。用该化合物处理的小鼠显示出视网膜结构损伤显著减少。与未处理的受试者相比，视网膜的重要层保持得更厚、更健康。

Even more impressive, visual function improved, as measured by electrical responses in the eye..

更令人印象深刻的是，视觉功能有所改善，这是通过眼睛的电反应测量得出的。

At the cellular level, the drug worked by stopping the buildup of harmful molecules and restoring the eye’s natural antioxidant defenses. It also reduced iron overload, a key trigger for ferroptosis.

在细胞层面，该药物通过阻止有害分子的积累并恢复眼睛的天然抗氧化防御来发挥作用。它还减少了铁过载，这是铁死亡的关键诱因。

A Key Molecular Pathway Identified

一个关键分子通路被识别

The study uncovered a crucial biological pathway behind the damage. A protein called EGR1 was found to play a central role in triggering cell death. When activated, EGR1 increases another protein, p53, which then suppresses a protective molecule known as xCT.

研究揭示了导致损伤的关键生物学通路。一种名为EGR1的蛋白质被发现是触发细胞死亡的核心因素。当EGR1被激活时，它会增加另一种蛋白质p53的水平，而p53则会抑制一种名为xCT的保护性分子。

This chain reaction weakens the cell’s ability to fight oxidative stress, leading to ferroptosis.

这种链式反应削弱了细胞抵抗氧化应激的能力，导致铁死亡。

Liproxstatin-1 interrupts this process. It reduces EGR1 and p53 activity while restoring xCT levels, effectively shutting down the destructive pathway. When researchers directly blocked EGR1 using genetic techniques, they observed similar protective effects, confirming its importance.

Liproxstatin-1中断了这一过程。它减少EGR1和p53的活性，同时恢复xCT水平，有效关闭了破坏性通路。当研究人员使用基因技术直接阻断EGR1时，他们观察到了类似的保护效果，证实了其重要性。

Reduced Inflammation and Oxidative Damage

减少炎症和氧化损伤

Beyond preventing cell death, the compound also reduced inflammation in the retina. Activated immune cells and stress-related proteins were significantly lower in treated subjects. This suggests the drug not only protects cells but

除了防止细胞死亡外，该化合物还减少了视网膜的炎症。在治疗对象中，活化的免疫细胞和与压力相关的蛋白质显著降低。这表明该药物不仅可以保护细胞，而且

also calms the damaging environment inside the eye.

同时还能平息眼睛内部的有害环境。

Markers of oxidative stress and lipid damage were dramatically reduced, while protective proteins were restored. This combination of effects provides a strong defense against multiple forms of injury.

氧化应激和脂质损伤的标志物显著减少，而保护性蛋白质得以恢复。这种多重效应的组合为抵御多种形式的损伤提供了强有力的防御。

What This Means for Future Treatments

这对未来治疗的意义

The findings suggest that Liproxstatin-1 or similar drugs could form the basis of new treatments for glaucoma and other vision-threatening conditions. By targeting ferroptosis at its source, scientists may finally have a way to slow or even prevent irreversible blindness.

研究结果表明，Liproxstatin-1 或类似药物可能成为治疗青光眼和其他威胁视力疾病的新方法的基础。通过从源头上靶向铁死亡，科学家们或许终于找到了减缓甚至预防不可逆失明的方法。

The research was conducted by scientists from the State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, and the Guangdong Provincial Key Laboratory of Ophthalmology Visual Science in Guangzhou, China.

这项研究由中山大学中山眼科中心、眼科学国家重点实验室以及广东省眼科视觉科学重点实验室的科学家在广州进行。

Conclusion

结论

This study provides compelling evidence that ferroptosis is a major driver of retinal damage and vision loss, and that targeting it can deliver meaningful protection. By identifying the EGR1–p53–xCT pathway as a critical control point, researchers have opened the door to highly targeted therapies. The ability of Liproxstatin-1 to preserve both retinal structure and function, reduce inflammation, and restore antioxidant balance highlights its strong clinical potential.

这项研究提供了有力的证据，表明铁死亡是视网膜损伤和视力丧失的主要驱动因素，而针对它进行干预可以提供显著的保护。通过将EGR1–p53–xCT通路确定为关键控制点，研究人员为高度针对性的治疗打开了大门。Liproxstatin-1在保护视网膜结构和功能、减轻炎症以及恢复抗氧化平衡方面的能力突显了其强大的临床潜力。

While further human studies are needed, these findings mark a significant step toward preventing blindness in millions of people worldwide..

虽然还需要进行更多的人体研究，但这些发现标志着在预防全球数百万人失明方面迈出了重要的一步。

The study findings were published in the peer reviewed journal: Antioxidants.

研究结果发表在同行评审期刊《抗氧化剂》上。

https://www.mdpi.com/2076-3921/15/3/391

For the latest on treating retinal injury, keep on logging to Thailand

为了获取治疗视网膜损伤的最新信息，请继续登录泰国。

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