Key result
12-LOX inhibition protects against diabetic retinopathy progression by reducing ROS generation in preclinical models.
Answers are grounded in this paper and cite their sources.
PURPOSE: Abnormal lipid metabolism has been proved to be implicated in the complex pathogenesis of diabetic retinopathy (DR). 12-lipoxygenase (12-LOX) is a member of lipoxygenase family responsible for the oxygenation of cellular polyunsaturated fatty acids to produce lipid mediators which modulate cell inflammation. This review explores the role of 12-lipoxygenase and its products in the pathogenesis of DR. METHODS: A comprehensive medical literature search was conducted on PubMed till September 2021. RESULTS: Emerging evidence has demonstrated that 12-LOX and its main product 12- hydroxyeicosatetraenoic acid (12-HETE) activate retinal cells, especially retinal vascular endothelial cells, through the activation of NADPH oxidase and the subsequent generation of reactive oxygen species (ROS), mediating multiple pathological changes during DR. Genetic deletion or pharmacological inhibition models of 12-LOX in mice show protection from DR. CONCLUSION: 12-LOX and its product 12-HETE take important part in DR pathogenesis and show their potential as future therapeutic targets for DR. Further studies are needed on the specific mechanism including 12-LOX pathway related molecules, 12-HETE receptors and downstream signaling pathways.
No takes yet. Share an insight, caveat, or question.
Chen et al. (2022) conducted a review in Diabetic retinopathy. 12-lipoxygenase (12-LOX) and 12-HETE was evaluated on Pathogenesis and progression of diabetic retinopathy. 12-lipoxygenase and its metabolite 12-HETE mediate pathological changes in diabetic retinopathy through ROS generation, while 12-LOX deletion or inhibition in mice shows protection.
Synapse has enriched 10 related papers. Consider them for comparative context: