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The mutation in ALDH4A1 leads to the accumulation of pyrroline-5-carboxylate (P5C) in the mitochondria, which can react with PLP to cause PLP deficiency in the brain and can also be converted to proline, resulting in elevated plasma proline levels (Fig

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Research using high-glucose-injured human retinal pigment epithelial cells (ARPE-19) showed Epithalon treatment restored impaired wound healing, reduced intracellular reactive oxygen species accumulation, and increased antioxidant gene expression

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