Hepatic retinopathy from a biochemical perspective
DOI:
https://doi.org/10.52556/2587-3873.2025.2(104).21Keywords:
hepatic retinopathy, Ammonia, Müller cells, oxidativestress, mitochondrial dysfunction, Energy metabolismAbstract
Hepatic retinopathy (HR) represents an extrahepatic manifestation observed in the context of advanced liver diseases, rooted in a complex interdependence between systemic metabolic dysfunctions and local biochemical processes within the retina. Ammonia toxicity, oxidative stress, neurotransmitter imbalances, and energy dysfunction are central to the pathogenesis of this complication. A comprehensive literature review was conducted, analyzing scientific publications from the last 30 years, retrieved from PubMed, Scopus, and Web of Science databases. Out of a total of 40 articles, 17 relevant studies focusing on biochemical alterations in hepatic retinopathy were selected for analysis. Depending on its etiology, HR involves multiple pathobiochemical pathways, including ammonia accumulation, impaired detoxification via glutamine synthetase, and disrupted glutamate and GABA metabolism, affecting both neurotransmission and retinal homeostasis. Over time, Müller cells develop compensatory morphological and biochemical changes, further depleting glutamate levels. Hyperammonemia induces the production of reactive oxygen species, while the retinal antioxidant system becomes insufficient. Mitochondrial dysfunction compromises ATP production, and β-oxidation of fatty acids represents an additional affected metabolic pathway, contributing to progressive visual impairment. HR reflects a multisystemic complication that requires complex therapeutic approaches aimed at reducing hyperammonemia, correcting oxidative stress, supporting mitochondrial function, and restoring neurotransmitter balance. A detailed understanding of these mechanisms offers new perspectives for prevention and personalized treatment.
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