{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:25:59Z","timestamp":1790727959736,"version":"4.1.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,5,6]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      The\n                      <jats:styled-content style=\"fixed-case\">NLR<\/jats:styled-content>\n                      family, pyrin domain containing 3 (\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3) inflammasome is an interleukin (\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      )\u20101\u03b2 and\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u201018 cytokine processing complex that is activated in inflammatory conditions. The role of the\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3 inflammasome in the pathogenesis of atherosclerosis and myocardial infarction is not fully understood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Atherosclerotic plaques were analyzed for transcripts of the\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3 inflammasome, and for\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u20101\u03b2 release. The Swedish First\u2010ever myocardial Infarction study in Ac\u2010county (\n                      <jats:styled-content style=\"fixed-case\">FIA<\/jats:styled-content>\n                      ) cohort consisting of\n                      <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                      from 555 myocardial infarction patients and 1016 healthy individuals was used to determine the frequency of 4 single nucleotide polymorphisms (\n                      <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>\n                      s) from the downstream regulatory region of\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3. Expression of\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3, Apoptosis\u2010associated speck\u2010like protein containing a\n                      <jats:styled-content style=\"fixed-case\">CARD<\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      ), caspase\u20101 (\n                      <jats:styled-content style=\"fixed-case\">CASP<\/jats:styled-content>\n                      1),\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      1B, and\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      18\n                      <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n                      was significantly increased in atherosclerotic plaques compared to normal arteries. The expression of\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3\n                      <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n                      was significantly higher in plaques of symptomatic patients when compared to asymptomatic ones.\n                      <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                      68\u2010positive macrophages were observed in the same areas of atherosclerotic lesions as\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3 and\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      expression. Occasionally, expression of\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3 and\n                      <jats:styled-content style=\"fixed-case\">ASC<\/jats:styled-content>\n                      was also present in smooth muscle cells. Cholesterol crystals and\n                      <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n                      induced\n                      <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                      \u20101\u03b2 release from lipopolysaccharide\u2010primed human atherosclerotic lesion plaques. The minor alleles of the variants rs4266924, rs6672995, and rs10733113 were associated with\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3\n                      <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n                      levels in peripheral blood mononuclear cells but not with the risk of myocardial infarction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Our results indicate a possible role of the\n                      <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                      3 inflammasome and its genetic variants in the pathogenesis of atherosclerosis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.115.003031","type":"journal-article","created":{"date-parts":[[2016,5,23]],"date-time":"2016-05-23T12:25:46Z","timestamp":1464006346000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":263,"title":["NLRP3 Inflammasome Expression and Activation in Human Atherosclerosis"],"prefix":"10.1161","volume":"5","author":[{"given":"Geena","family":"Paramel Varghese","sequence":"first","affiliation":[{"name":"Cardiovascular Research Centre, Faculty of Medicine and Health, School of Health and Medical Sciences, \u00d6rebro University, \u00d6rebro, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lasse","family":"Folkersen","sequence":"additional","affiliation":[{"name":"Department of Medicine and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rona J.","family":"Strawbridge","sequence":"additional","affiliation":[{"name":"Department of Medicine and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bente","family":"Halvorsen","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway"},{"name":"Institute of Clinical Medicine, University of Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arne","family":"Yndestad","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway"},{"name":"K.G. Jebsen Inflammatory Research Center, University of Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trine","family":"Ranheim","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway"},{"name":"Institute of Clinical Medicine, University of Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirsten","family":"Krohg\u2010S\u00f8rensen","sequence":"additional","affiliation":[{"name":"Department of Thoracic and Cardiovascular Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mona","family":"Skjelland","sequence":"additional","affiliation":[{"name":"Department of Neurology, Oslo University Hospital Rikshospitalet, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Terje","family":"Espevik","sequence":"additional","affiliation":[{"name":"Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P\u00e5l","family":"Aukrust","sequence":"additional","affiliation":[{"name":"Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway"},{"name":"Section\u00a0of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway"},{"name":"Institute of Clinical Medicine, University of Oslo, Norway"},{"name":"K.G. 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