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dc.contributor.authorde los Reyes García, Ascensión M.
dc.contributor.authorRivera Caravaca, José Miguel
dc.contributor.authorZapata Martínez, Laura
dc.contributor.authorÁguila, Sonia
dc.contributor.authorVéliz Martínez, Andrea
dc.contributor.authorGarcía Barberá, Nuria
dc.contributor.authorGil Pérez, Pablo
dc.contributor.authorGuijarro Carrillo, Pedro J.
dc.contributor.authorOrenes Piñero, Esteban
dc.contributor.authorLópez García, Cecilia
dc.contributor.authorLozano, María L.
dc.contributor.authorMarín, Francisco
dc.contributor.authorMartínez, Constantino
dc.contributor.authorGonzález Conejero, Rocío
dc.date.accessioned2026-01-26T10:58:23Z
dc.date.available2026-01-26T10:58:23Z
dc.date.issued2022-07-20
dc.identifier.citationde Los Reyes-García AM, Rivera-Caravaca JM, Zapata-Martínez L, Águila S, Véliz-Martínez A, García-Barberá N, Gil-Perez P, Guijarro-Carrillo PJ, Orenes-Piñero E, López-García C, Lozano ML, Marín F, Martínez C, González-Conejero R. MiR-146a Contributes to Thromboinflammation and Recurrence in Young Patients with Acute Myocardial Infarction. J Pers Med. 2022 Jul 20;12(7):1185. doi: 10.3390/jpm12071185. PMID: 35887682; PMCID: PMC9318357es
dc.identifier.urihttp://hdl.handle.net/10952/10706
dc.description.abstractAbstract: Studies on older patients have established notable conceptual changes in the etiopatho genesis of acute coronary syndrome (ACS), but little is known about this disease in young patients ( Q4 more frequently had a history of previous stroke (6.1% vs. 1.6%). In turn, rs2431697 did not confer increased risk for the onset of ACS, but T carriers had significantly higher levels of NET markers. By groups, we found that cfDNA levels were similarly higher in all patients, but citH3–DNA was especially higher in G1, suggesting that in plasma, this marker may be attenuated over time. Finally, patients from G2 with the worst markers (cfDNA and citH3–DNA > Q2 and T allele) had a two-fold increased risk of a new ischemic event at 2-year follow-up. In conclusion, our data confirm that ACS is younger onset with thromboinflammatory disease. In addition, these data consolidate rs2431697 as a silent proinflammatory factor predisposing to NETosis, and to a higher rate of adverse events in different cardiovascular diseaseses
dc.description.abstractResumen: Los estudios en pacientes de mayor edad han establecido cambios conceptuales importantes en la etiopatogenia del síndrome coronario agudo (SCA), pero se conoce poco sobre esta enfermedad en pacientes jóvenes. El cuartil 4 (Q4) presentó con mayor frecuencia antecedentes de ictus previo (6,1 % frente a 1,6 %). Por otro lado, el polimorfismo rs2431697 no se asoció con un mayor riesgo de aparición de SCA, aunque los portadores del alelo T mostraron niveles significativamente más altos de marcadores de NETs. Por grupos, se observó que los niveles de cfDNA eran similares y elevados en todos los pacientes, mientras que citH3–DNA fue especialmente mayor en el grupo 1 (G1), lo que sugiere que, en plasma, este marcador podría atenuarse con el tiempo. Finalmente, los pacientes del grupo 2 (G2) con los peores marcadores (cfDNA y citH3–DNA > Q2 y alelo T) presentaron un riesgo doble de un nuevo evento isquémico a los 2 años de seguimiento. En conclusión, nuestros datos confirman que el SCA en pacientes jóvenes se caracteriza por ser una enfermedad tromboinflamatoria. Además, estos datos consolidan a rs2431697 como un factor proinflamatorio silencioso que predispone a la NETosis y a una mayor tasa de eventos adversos en diversas enfermedades cardiovasculares.es
dc.language.isoenes
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectmiR-146aes
dc.subjectThromboinflammationes
dc.subjectAcute Myocardial infarctiones
dc.subjectRecurrencees
dc.subjectYoung Patientses
dc.titleMiR-146a Contributes to Thromboinflammation and Recurrence in Young Patients with Acute Myocardial Infarctiones
dc.typejournal articlees
dc.rights.accessRightsopen accesses
dc.journal.titleJournal of Personalized Medicinees
dc.volume.number12es
dc.issue.number1185es
dc.description.disciplineMedicinaes
dc.identifier.doi10.3390/jpm12071185.es


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