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Erythropoietin in Glaucoma: From Mechanism to Therapy

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MDPI
DOI: 10.3390/ijms24032985

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erythropoietin; neuroprotection; retinal ganglion cell; glaucoma

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Glaucoma, the second leading cause of blindness worldwide, can result in irreversible vision loss. The disease is complex, with various factors contributing to its development, such as ischemia, oxidative stress, neurotropic factor deprivation, and neuron excitotoxicity. Erythropoietin (EPO), a hormone that stimulates erythropoiesis in response to hypoxia, has been found to have neuroprotective effects and may be a potential treatment for rescuing retinal ganglion cells in glaucoma. This article explores the relationship between EPO and glaucoma and summarizes preclinical experiments using EPO, offering a different perspective on the incurability of glaucoma.
Glaucoma can cause irreversible vision loss and is the second leading cause of blindness worldwide. The disease mechanism is complex and various factors have been implicated in its pathogenesis, including ischemia, excessive oxidative stress, neurotropic factor deprivation, and neuron excitotoxicity. Erythropoietin (EPO) is a hormone that induces erythropoiesis in response to hypoxia. However, studies have shown that EPO also has neuroprotective effects and may be useful for rescuing apoptotic retinal ganglion cells in glaucoma. This article explores the relationship between EPO and glaucoma and summarizes preclinical experiments that have used EPO to treat glaucoma, with an aim to provide a different perspective from the current view that glaucoma is incurable.

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