This therapeutic potential is highly significant, as DM impairs the TM through persistent hyperglycaemia, which enhances mitochondrial ROS production, creating a highly profibrotic microenvironment [ 63 , 64 ].
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The Sigma-1 Receptor Agonist Fluvoxamine Is Protective in Hyperglycaemia-Induced Dysfunction of Trabecular Meshwork Cells.
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