ArticleOxidative medicine and cellular longevity2014
Polyol pathway exacerbated ischemia/reperfusion-induced injury in steatotic liver.
Article in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Metabolism Dysregulation in Retinal Diseases and Related Therapies.Antioxidants (Basel, Switzerland) · 2022Review
- The Inhibition of Aldose Reductase Accelerates Liver Regeneration through Regulating Energy Metabolism.Oxidative medicine and cellular longevity · 2020Article
- Effect of Heat Stress on Sperm DNA: Protamine Assessment in Ram Spermatozoa and Testicle.Oxidative medicine and cellular longevity · 2018Article
- Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury.BioMed research international · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
backgroundThe polyol pathway, a bypass pathway of glucose metabolism initiated by aldose reductase (AR), has been shown to play an important role in mediating tissue ischemia/reperfusion (I/R) impairment recently. Here, we investigated how and why this pathway might affect the fatty liver following I/R.
methodsTwo opposite models were created: mice with high-fat-diet-induced liver steatosis were treated with aldose reductase inhibition (ARI) and subsequent I/R; and AR-overexpressing L02 hepatocytes were sequentially subjected to steatosis and hypoxia/reoxygenation. We next investigated (a) the hepatic injuries, including liver function, histology, and hepatocytes apoptosis/necrosis; (b) the NAD(P)(H) contents, redox status, and mitochondrial function; and (c) the flux through the caspase-dependent apoptosis pathway.
resultsAR-inhibition in vivo markedly attenuated the I/R-induced liver injuries, maintained the homeostasis of NAD(P)(H) contents and redox status, and suppressed the caspase-dependent apoptosis pathway. Correspondingly, AR overexpression in vitro presented the opposite effects.
conclusionThe flux through the polyol pathway may render steatotic liver greater vulnerability to I/R. Interventions targeting this pathway might provide a novel adjunctive approach to protect fatty liver from ischemia.
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