Key result
Thioredoxin-1 protects against ox-LDL-induced endothelial injury by suppressing NADPH oxidase and inflammatory pathways.
Why the study?
Oxidized low-density lipoprotein and related reactive oxygen species contribute to endothelial injury in atherosclerosis, and the role of thioredoxin-1 in this process requires summarization.
Thioredoxin-1 acts as a key intracellular redox regulator that may protect against ox-LDL-induced endothelial injury in atherosclerosis.
Does not alter clinical management of atherosclerosis; leaves open thioredoxin-1 as a therapeutic target.
Atherosclerosis is a chronic inflammation disease that is initiated by endothelial cell injury.Hyperlipidemia is an independent risk factor for atherosclerosis.Oxidized low-density lipoprotein (ox-LDL) is a major component of hyperlipidemia and contributes to atherosclerosis.Ox-LDL and ox-LDLrelated reactive oxygen species (ROS) and inflammation have deleterious effects on vascular endothelial cells.Previous studies have demonstrated that thioredoxin-1 (Trx) is one of the key regulators of intracellular redox, which may play a role in the pathogenesis of atherosclerosis.This review will summarize the protective mechanisms of Trx on endothelial injury induced by ox-LDL.
No takes yet. Share an insight, caveat, or question.
Beidong Chen (2018) conducted a review in Atherosclerosis. Thioredoxin-1 was evaluated. Thioredoxin-1 protects against ox-LDL-induced atherosclerotic endothelial injury by reducing NADPH oxidase activity, regulating AP-1 and Smad3 pathways, and inhibiting inflammatory protein expression.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: