FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4387336048> ?p ?o ?g. }

• W4387336048 endingPage "102906" @default.
• W4387336048 startingPage "102906" @default.
• W4387336048 abstract "Microvascular endothelial damage caused by intestinal ischemia‒reperfusion (II/R) is a primary catalyst for microcirculation dysfunction and enterogenous infection. Previous studies have mainly focused on how neutrophil extracellular traps (NETs) and ferroptosis cause intestinal epithelial injury, and little attention has been given to how NETs, mainly from circulatory neutrophils, affect intestinal endothelial cells during II/R. This study aimed to unravel the mechanisms through which NETs cause intestinal microvascular dysfunction. We first detected heightened local NET infiltration around the intestinal microvasculature, accompanied by increased endothelial cell ferroptosis, resulting in microcirculation dysfunction in both human and animal II/R models. However, the administration of the ferroptosis inhibitor ferrostatin-1 or the inhibition of NETs via neutrophil-specific peptidylarginine deiminase 4 (Pad4) deficiency led to positive outcomes, with reduced intestinal endothelial ferroptosis and microvascular function recovery. Moreover, RNA-seq analysis revealed a significant enrichment of mitophagy- and ferroptosis-related signaling pathways in HUVECs incubated with NETs. Mechanistically, elevated NET formation induced Fundc1 phosphorylation at Tyr18 in intestinal endothelial cells, which led to mitophagy inhibition, mitochondrial quality control imbalance, and excessive mitochondrial ROS generation and lipid peroxidation, resulting in endothelial ferroptosis and microvascular dysfunction. Nevertheless, using the mitophagy activator urolithin A or AAV-Fundc1 transfection could reverse this process and ameliorate microvascular damage. We first demonstrate that increased NETosis could result in intestinal microcirculatory dysfunction and conclude that suppressed NET formation can mitigate intestinal endothelial ferroptosis by improving Fundc1-dependent mitophagy. Targeting NETs could be a promising approach for treating II/R-induced intestinal microcirculatory dysfunction." @default.
• W4387336048 created "2023-10-05" @default.
• W4387336048 creator A5001245936 @default.
• W4387336048 creator A5006075933 @default.
• W4387336048 creator A5021984184 @default.
• W4387336048 creator A5027822882 @default.
• W4387336048 creator A5028497573 @default.
• W4387336048 creator A5040502531 @default.
• W4387336048 creator A5047722125 @default.
• W4387336048 creator A5058531296 @default.
• W4387336048 creator A5066252438 @default.
• W4387336048 creator A5067253563 @default.
• W4387336048 creator A5073531557 @default.
• W4387336048 date "2023-11-01" @default.
• W4387336048 modified "2023-10-16" @default.
• W4387336048 title "Neutrophil extracellular traps drive intestinal microvascular endothelial ferroptosis by impairing Fundc1-dependent mitophagy" @default.
• W4387336048 cites W1127532827 @default.
• W4387336048 cites W2049172731 @default.
• W4387336048 cites W2059699981 @default.
• W4387336048 cites W2087485016 @default.
• W4387336048 cites W2104934425 @default.
• W4387336048 cites W2115480752 @default.
• W4387336048 cites W2571646432 @default.
• W4387336048 cites W2735250338 @default.
• W4387336048 cites W2786765075 @default.
• W4387336048 cites W2904940732 @default.
• W4387336048 cites W2911996561 @default.
• W4387336048 cites W2915164054 @default.
• W4387336048 cites W2922365089 @default.
• W4387336048 cites W2971698053 @default.
• W4387336048 cites W2972917954 @default.
• W4387336048 cites W2980622391 @default.
• W4387336048 cites W3010943409 @default.
• W4387336048 cites W3012782412 @default.
• W4387336048 cites W3027661062 @default.
• W4387336048 cites W3048787877 @default.
• W4387336048 cites W3118831406 @default.
• W4387336048 cites W3118865203 @default.
• W4387336048 cites W3135029476 @default.
• W4387336048 cites W3138795306 @default.
• W4387336048 cites W3158475749 @default.
• W4387336048 cites W3172161742 @default.
• W4387336048 cites W3191105548 @default.
• W4387336048 cites W3209998537 @default.
• W4387336048 cites W3212931987 @default.
• W4387336048 cites W3213673096 @default.
• W4387336048 cites W4200139183 @default.
• W4387336048 cites W4200275200 @default.
• W4387336048 cites W4213442676 @default.
• W4387336048 cites W4220753472 @default.
• W4387336048 cites W4223423231 @default.
• W4387336048 cites W4223505641 @default.
• W4387336048 cites W4223567523 @default.
• W4387336048 cites W4224700161 @default.
• W4387336048 cites W4281697000 @default.
• W4387336048 cites W4283381540 @default.
• W4387336048 cites W4285109083 @default.
• W4387336048 cites W4294218079 @default.
• W4387336048 cites W4294584780 @default.
• W4387336048 cites W4294606674 @default.
• W4387336048 cites W4306750531 @default.
• W4387336048 cites W4307552150 @default.
• W4387336048 cites W4308158341 @default.
• W4387336048 cites W4318815931 @default.
• W4387336048 cites W4319160267 @default.
• W4387336048 cites W4321487204 @default.
• W4387336048 cites W4324009186 @default.
• W4387336048 cites W4360954530 @default.
• W4387336048 cites W4362456036 @default.
• W4387336048 cites W4362657000 @default.
• W4387336048 cites W4364379667 @default.
• W4387336048 cites W4366083072 @default.
• W4387336048 cites W4372291697 @default.
• W4387336048 cites W4375955051 @default.
• W4387336048 cites W4376278454 @default.
• W4387336048 cites W4378173510 @default.
• W4387336048 cites W4386020136 @default.
• W4387336048 doi "https://doi.org/10.1016/j.redox.2023.102906" @default.
• W4387336048 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37812880" @default.
• W4387336048 hasPublicationYear "2023" @default.
• W4387336048 type Work @default.
• W4387336048 citedByCount "0" @default.
• W4387336048 crossrefType "journal-article" @default.
• W4387336048 hasAuthorship W4387336048A5001245936 @default.
• W4387336048 hasAuthorship W4387336048A5006075933 @default.
• W4387336048 hasAuthorship W4387336048A5021984184 @default.
• W4387336048 hasAuthorship W4387336048A5027822882 @default.
• W4387336048 hasAuthorship W4387336048A5028497573 @default.
• W4387336048 hasAuthorship W4387336048A5040502531 @default.
• W4387336048 hasAuthorship W4387336048A5047722125 @default.
• W4387336048 hasAuthorship W4387336048A5058531296 @default.
• W4387336048 hasAuthorship W4387336048A5066252438 @default.
• W4387336048 hasAuthorship W4387336048A5067253563 @default.
• W4387336048 hasAuthorship W4387336048A5073531557 @default.
• W4387336048 hasBestOaLocation W43873360481 @default.
• W4387336048 hasConcept C123012128 @default.
• W4387336048 hasConcept C126322002 @default.
• W4387336048 hasConcept C12722491 @default.

• next