FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022689308> ?p ?o ?g. }

• W2022689308 endingPage "786" @default.
• W2022689308 startingPage "782" @default.
• W2022689308 abstract "En la actualidad se acepta que la aterosclerosis es un proceso inflamatorio crónico de la pared arterial asociado con la presencia de diversos factores de riesgo. Desde las fases iniciales hasta la rotura de una placa aterosclerótica vulnerable, el estado de «microinflamación vascular» desempeña un papel fisiopatológico relevante. Diversos marcadores inflamatorios (proteína C reactiva, citocinas, moléculas de adhesión) han demostrado un papel importante en este proceso inflamatorio. Evidencias clínicas y experimentales también indican que la ciclooxigenasa 2 (COX-2), una enzima que cataliza la generación de prostaglandinas a partir del ácido araquidónico, también contribuye al desarrollo de la lesion aterosclerótica. Nuestro grupo ha demostrado recientemente la asociación de la prostaglandina E2 (un metabolito derivado de la COX-2 en monocitos) con factores de riesgo y el espesor íntima-media de la carótida en un grupo de sujetos asintomáticos, lo que indicaría que la vía COX-2/prostaglandina E2 podría desempeñar un papel en la aterosclerosis y representar una nueva diana terapéutica. Desde el punto de vista teórico, los inhibidores selectivos de la COX-2, denominados genéricamente «coxib» (celecoxib, rofecoxib, valdecoxib, lumiracoxib, etc.), podrían ser útiles como fármacos antiinflamatorios en este proceso, sin los efectos secundarios de la aspirina u otros antiinflamatorios no esteroideos. Sin embargo, diversos estudios clínicos señalan que pueden inducir un aumento de complicaciones cardiovasculares, por alteración del equilibrio tromboxano/prostaciclina, por lo que su uso debe restringirse, especialmente en pacientes con riesgo aterosclerótico alto. It is now widely accepted that atherosclerosis is a complex chronic inflammatory disorder of the arterial tree associated with several risk factors. From the initial phases to eventual rupture of vulnerable atherosclerotic plaques, a low-grade inflammation, also termed microinflammation, appears to play a key pathogenetic role. Systemic inflammatory markers (C reactive protein, cytokines adhesion molecules) also play a role in this process. Experimental and clinical evidence suggests that cyclooxygenase-2 (COX-2), an enzyme which catalyzes the generation of prostaglandins from arachidonic acid, also contributes to lesion formation. Recent reports by our group have demonstrated increased monocyte COX-2 activity and the production of prostaglandin E2 in relation to cardiovascular risk factors and subclinical atherosclerosis in asymptomatic subjects. Our findings support the notion that the COX-2/prostaglandin E2 axis may have a role, raising the cuestion as to whether its selective inhibition might be an attractive therapeutic target in atherosclerosis. COX-2 inhibitors, collectively called «coxibs» (celecoxib, rofecoxib, valdecoxib, lumiracoxib, etc), held a promise as anti-inflammatory drugs without the some of the side effects of aspirin or non steroidal anti-inflammatory agents. However, clinical studies raise several clinically relevant questions as to their beneficial role in atherosclerosis prevention, because of increased thrombogenicity and cardiovascular risk, and therefore coxibs should be restricted in atherosclerosis-prone patients." @default.
• W2022689308 created "2016-06-24" @default.
• W2022689308 creator A5017448314 @default.
• W2022689308 creator A5061782816 @default.
• W2022689308 creator A5083600076 @default.
• W2022689308 date "2006-05-01" @default.
• W2022689308 modified "2023-09-27" @default.
• W2022689308 title "Ciclooxigenasa 2: ¿una nueva diana terapéutica en la aterosclerosis?" @default.
• W2022689308 cites W1539392991 @default.
• W2022689308 cites W1586509612 @default.
• W2022689308 cites W1587059515 @default.
• W2022689308 cites W1666619344 @default.
• W2022689308 cites W1670371184 @default.
• W2022689308 cites W1893697461 @default.
• W2022689308 cites W1964797510 @default.
• W2022689308 cites W1975248941 @default.
• W2022689308 cites W1976915409 @default.
• W2022689308 cites W1983707947 @default.
• W2022689308 cites W1987031993 @default.
• W2022689308 cites W1997042650 @default.
• W2022689308 cites W1998976537 @default.
• W2022689308 cites W2001162433 @default.
• W2022689308 cites W2004916700 @default.
• W2022689308 cites W2014184499 @default.
• W2022689308 cites W2016071225 @default.
• W2022689308 cites W2020563114 @default.
• W2022689308 cites W2024233889 @default.
• W2022689308 cites W2024237851 @default.
• W2022689308 cites W2024289681 @default.
• W2022689308 cites W2025653938 @default.
• W2022689308 cites W2032485049 @default.
• W2022689308 cites W2037341294 @default.
• W2022689308 cites W2037405899 @default.
• W2022689308 cites W2042928324 @default.
• W2022689308 cites W2044706016 @default.
• W2022689308 cites W2046501054 @default.
• W2022689308 cites W2053230224 @default.
• W2022689308 cites W2054872303 @default.
• W2022689308 cites W2055691692 @default.
• W2022689308 cites W2057685090 @default.
• W2022689308 cites W2061857216 @default.
• W2022689308 cites W2063144963 @default.
• W2022689308 cites W2063727271 @default.
• W2022689308 cites W2064663457 @default.
• W2022689308 cites W2066963386 @default.
• W2022689308 cites W2077369709 @default.
• W2022689308 cites W2084120431 @default.
• W2022689308 cites W2087880770 @default.
• W2022689308 cites W2088179332 @default.
• W2022689308 cites W2096198355 @default.
• W2022689308 cites W2096422139 @default.
• W2022689308 cites W2098657147 @default.
• W2022689308 cites W2105605377 @default.
• W2022689308 cites W2107791153 @default.
• W2022689308 cites W2110809844 @default.
• W2022689308 cites W2113546175 @default.
• W2022689308 cites W2113892902 @default.
• W2022689308 cites W2120087849 @default.
• W2022689308 cites W2123578563 @default.
• W2022689308 cites W2126853519 @default.
• W2022689308 cites W2129333373 @default.
• W2022689308 cites W2131732462 @default.
• W2022689308 cites W2135393211 @default.
• W2022689308 cites W2136385901 @default.
• W2022689308 cites W2136952749 @default.
• W2022689308 cites W2137220230 @default.
• W2022689308 cites W2140199200 @default.
• W2022689308 cites W2143378100 @default.
• W2022689308 cites W2146478455 @default.
• W2022689308 cites W2148744880 @default.
• W2022689308 cites W2149233326 @default.
• W2022689308 cites W2152021373 @default.
• W2022689308 cites W2153853877 @default.
• W2022689308 cites W2158131645 @default.
• W2022689308 cites W2158968701 @default.
• W2022689308 cites W2159087408 @default.
• W2022689308 cites W2163149796 @default.
• W2022689308 cites W2163756514 @default.
• W2022689308 cites W2330496155 @default.
• W2022689308 cites W4240520654 @default.
• W2022689308 cites W4240900378 @default.
• W2022689308 cites W4243831921 @default.
• W2022689308 cites W4256475235 @default.
• W2022689308 doi "https://doi.org/10.1157/13089104" @default.
• W2022689308 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16792983" @default.
• W2022689308 hasPublicationYear "2006" @default.
• W2022689308 type Work @default.
• W2022689308 sameAs 2022689308 @default.
• W2022689308 citedByCount "5" @default.
• W2022689308 countsByYear W20226893082022 @default.
• W2022689308 crossrefType "journal-article" @default.
• W2022689308 hasAuthorship W2022689308A5017448314 @default.
• W2022689308 hasAuthorship W2022689308A5061782816 @default.
• W2022689308 hasAuthorship W2022689308A5083600076 @default.
• W2022689308 hasBestOaLocation W20226893082 @default.
• W2022689308 hasConcept C138885662 @default.
• W2022689308 hasConcept C15708023 @default.
• W2022689308 hasConcept C71924100 @default.

• next