ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Myocardial ischemia-reperfusion (MI/R) injury remains a critical challenge in cardiovascular therapeutics, with metabolic-inflammatory signaling axis emerging as a critical mediator of pathological outcomes. Yet, the specific metabolic pathways interplay with inflammation to exacerbate MI/R injury remain poorly defined. Here we verify that NETosis of neutrophils is an initiative and causal factor in driving MI/R injury, specifically, platelet activating factor (PAF) secreted by cardiomyocytes during MI/R, drives neutrophil extracellular traps (NETs) formation and subsequent NETosis. Increased expression of PAF synthesis enzyme PLA2G6 explains excessive production of PAF. PAF-induced NETosis requires gasdermin D (GSDMD) mediated pore-forming to facilitate NETs extrusion. Both inhibiting NETs and PAF synthesis significantly alleviate MI/R injury. We further identify dapagliflozin as a potent NETosis inhibitor that protects mice from MI/R injury in a sodium-glucose co-transporter 2 (SGLT2)-independent manner, which targets neutrophil gelatinase-associated lipocalin-2 (LCN2). Notably, increased serum PAF concentration in acute myocardial infarction patients with percutaneous coronary intervention was positively correlated with NETosis and myocardial injury indexes. Of interest, patients receiving dapagliflozin exhibited attenuated myocardial injury in comparison to those without dapagliflozin. Collectively, our study demonstrates PAF serves as a danger signal in triggering NETosis in early MI/R injury, and manipulating PAF-NETosis signal by dapagliflozin or LCN2 inhibitor might be effective in combating MI/R injury.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.