{"entity": "journal", "iuid": "51b394eb68224c2fa09d92eac2eb14b0", "timestamp": "2026-07-20T22:40:54.537Z", "links": {"self": {"href": "https://publications.scilifelab.se/journal/Heart.json"}, "display": {"href": "https://publications.scilifelab.se/journal/Heart"}}, "title": "Heart", "issn": "1468-201X", "issn-l": "1355-6037", "publications_count": 4, "publications": [{"entity": "publication", "iuid": "14fae7f53f414c66aa6903c0f026d037", "links": {"self": {"href": "https://publications.scilifelab.se/publication/14fae7f53f414c66aa6903c0f026d037.json"}, "display": {"href": "https://publications.scilifelab.se/publication/14fae7f53f414c66aa6903c0f026d037"}}, "title": "Circulating soluble LOX-1 and patient prognosis after an acute coronary syndrome.", "authors": [{"family": "Schiopu", "given": "Alexandru", "initials": "A", "orcid": "0000-0002-7587-5050", "researcher": {"href": "https://publications.scilifelab.se/researcher/c7d2edf9030a445583f692dc4d884b7f.json"}}, {"family": "Svedlund", "given": "Sara", "initials": "S"}, {"family": "Narasimhan", "given": "Gayathri", "initials": "G"}, {"family": "Juin Loong", "given": "Bi", "initials": "B"}, {"family": "Yndigegn", "given": "Troels", "initials": "T", "orcid": "0000-0002-8960-2125", "researcher": {"href": "https://publications.scilifelab.se/researcher/2c5f5069c767413eaa653581f7f0bfe9.json"}}, {"family": "Varma", "given": "Vijayalakshmi", "initials": "V"}, {"family": "Ongstad", "given": "Emily L", "initials": "EL"}, {"family": "Goncalves", "given": "Isabel", "initials": "I"}, {"family": "Coll\u00e9n", "given": "Anna", "initials": "A"}, {"family": "Nilsson", "given": "Jan", "initials": "J"}, {"family": "Gan", "given": "Li-Ming", "initials": "LM"}], "type": "journal article", "published": "2025-09-16", "journal": {"title": "Heart", "issn": "1468-201X", "issn-l": "1355-6037"}, "abstract": "The lectin-like oxidised low-density lipoprotein receptor-1 (LOX-1) mediates atherosclerotic plaque inflammation and vulnerability. On activation, LOX-1 sheds its extracellular domain into the circulation as soluble LOX-1 (sLOX-1). sLOX-1 is markedly elevated in patients with acute coronary syndrome (ACS).\n\nWe prospectively assessed the associations between plasma sLOX-1 and the development of heart failure (HF), major adverse cardiovascular events (MACE) and coronary and left ventricular (LV) dysfunction in two cohorts of patients with ACS. The first cohort comprised 524 patients recruited during the acute index event at the coronary care unit of Sk\u00e5ne University Hospital, Malm\u00f6, Sweden. The second cohort included 363 patients with ACS treated with acute percutaneous intervention at Sahlgrenska University Hospital, Gothenburg, Sweden. Additionally, we examined the anti-inflammatory effects of LOX-1 blockade in vitro using human umbilical vein endothelial cells (HUVECs).\n\nIn the first cohort, acute-phase sLOX-1 was associated with incident HF and MACE independently of cardiovascular risk factors, revascularisation and medication (HR per 1-SD sLOX-1 increase: 1.57 (95% CI: 1.10 to 2.23; p=0.012) for HF and 1.36 (1.08 to 1.71; p=0.009) for MACE). Elevated sLOX-1 was also associated with lower LV ejection fraction and accelerated remodelling, as measured by echocardiography at 1-year post-ACS. In the second cohort, sLOX-1 was negatively associated with left anterior descending coronary artery flow reserve and LV systolic function, and positively correlated with soluble markers of systemic inflammation and cardiac overload at 4 and 16 weeks post-ACS. In vitro, antibody-mediated LOX-1 blockade prevented oxidised low-density lipoprotein-induced HUVEC activation.\n\nElevated plasma sLOX-1 at baseline and during follow-up is associated with incident HF and MACE, as well as cardiac and coronary dysfunction in patients with ACS. As plasma sLOX-1 levels may reflect the intensity of LOX-1 expression on vascular and immune cells, these findings support LOX-1 as a potentially important therapeutic target to improve prognosis in patients with ACS.", "doi": "10.1136/heartjnl-2025-326315", "pmid": "40957671", "labels": {"Affinity Proteomics Uppsala": "Service"}, "xrefs": [{"db": "pii", "key": "heartjnl-2025-326315"}], "notes": [], "created": "2025-11-25T19:20:38.823Z", "modified": "2025-11-25T19:20:38.894Z"}, {"entity": "publication", "iuid": "bcd15fd6812c4d539ad51805dfafdbed", "links": {"self": {"href": "https://publications.scilifelab.se/publication/bcd15fd6812c4d539ad51805dfafdbed.json"}, "display": {"href": "https://publications.scilifelab.se/publication/bcd15fd6812c4d539ad51805dfafdbed"}}, "title": "Increased vascular endothelial growth factor D is associated with atrial fibrillation and ischaemic stroke.", "authors": [{"family": "Berntsson", "given": "John", "initials": "J", "orcid": "0000-0002-3464-5427", "researcher": {"href": "https://publications.scilifelab.se/researcher/d5e93b88f49142feb95ba600d71f66c7.json"}}, {"family": "Smith", "given": "J Gustav", "initials": "JG"}, {"family": "Johnson", "given": "Linda S B", "initials": "LSB"}, {"family": "S\u00f6derholm", "given": "Martin", "initials": "M"}, {"family": "Born\u00e9", "given": "Yan", "initials": "Y"}, {"family": "Melander", "given": "Olle", "initials": "O"}, {"family": "Orho-Melander", "given": "Marju", "initials": "M"}, {"family": "Nilsson", "given": "Jan", "initials": "J"}, {"family": "Engstr\u00f6m", "given": "Gunnar", "initials": "G"}], "type": "journal article", "published": "2019-04-00", "journal": {"title": "Heart", "issn": "1468-201X", "issn-l": "1355-6037", "volume": "105", "issue": "7", "pages": "553-558"}, "abstract": "Vascular endothelial growth factor D (VEGF-D) has important functions in lymphangiogenesis and angiogenesis. High plasma levels of VEGF-D have been associated with incidence of heart failure. The association of VEGF-D with atrial fibrillation (AF) and stroke is unclear and we hypothesised that VEGF-D could also be associated with incidence of AF and ischaemic stroke.\n\nVEGF-D was measured in fasting blood samples of 4689 subjects (40% men) without a history of AF from the Malm\u00f6 Diet and Cancer Study, a prospective, population-based study in Sweden. Median age was 58 years (range 46-68). Cox regression analyses, adjusted for multiple risk factors, was used to assess AF and ischaemic stroke risk in relation to VEGF-D levels.\n\nDuring a median follow-up time of 20.6 years, there were 637 cases of incident AF and 322 cases of first ischaemic stroke. After adjustment, VEGF-D was significantly associated with AF (HR 1.13(95% CI 1.04 to 1.23) per 1 SD increase) and ischaemic stroke (HR 1.14(95% CI 1.02 to 1.28) per 1 SD). The association with ischaemic stroke was explained by an increased incidence of AF-related stroke. HRs per 1 SD were 1.34 (95% CI 1.04 to 1.71) for AF-related ischaemic stroke and 1.04 (95% CI 0.90 to 1.19) for ischaemic stroke without AF.\n\nIncreased VEGF-D concentrations were associated with AF and ischaemic stroke. The relationship with ischaemic stroke was more pronounced in subjects with a diagnosis of AF.", "doi": "10.1136/heartjnl-2018-313684", "pmid": "30327392", "labels": {"Clinical Biomarkers": "Service", "PLA and Single Cell Proteomics": "Service", "Affinity Proteomics Uppsala": "Service"}, "xrefs": [{"db": "pii", "key": "heartjnl-2018-313684"}], "notes": [], "created": "2020-01-23T15:57:17.613Z", "modified": "2023-04-14T13:55:58.496Z"}, {"entity": "publication", "iuid": "cad7ac8c65a143ce922d87d02dc1d5e5", "links": {"self": {"href": "https://publications.scilifelab.se/publication/cad7ac8c65a143ce922d87d02dc1d5e5.json"}, "display": {"href": "https://publications.scilifelab.se/publication/cad7ac8c65a143ce922d87d02dc1d5e5"}}, "title": "Discovery of new biomarkers for atrial fibrillation using a custom-made proteomics chip.", "authors": [{"family": "Lind", "given": "Lars", "initials": "L"}, {"family": "Sundstr\u00f6m", "given": "Johan", "initials": "J"}, {"family": "Stenemo", "given": "Markus", "initials": "M"}, {"family": "Hagstr\u00f6m", "given": "Emil", "initials": "E"}, {"family": "\u00c4rnl\u00f6v", "given": "Johan", "initials": "J"}], "type": "journal article", "published": "2017-03-00", "journal": {"title": "Heart", "issn": "1468-201X", "issn-l": "1355-6037", "volume": "103", "issue": "5", "pages": "377-382"}, "abstract": "Apart from several established clinical risk factors for atrial fibrillation (AF), a number of biomarkers have also been identified as potential risk factors for AF. None of these have so far been adopted in clinical practice.\n\nTo use a novel custom-made proteomics chip to discover new prognostic biomarkers for AF risk.\n\nIn two independent community-based cohorts (Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study (978 participants without AF, mean age 70.1 years, 50% women, median follow-up 10.0 years) and Uppsala Longitudinal Study of Adult Men (ULSAM) (n=725, mean age 77.5 years, median follow-up 7.9 years)), ninety-two plasma proteins were assessed at baseline by a proximity extension assay (PEA) chip. Of those, 85 proteins showed a call rate >70% in both cohorts.\n\nThirteen proteins were related to incident AF in PIVUS (148 events) using a false discovery rate of 5%. Of those, five were replicated in ULSAM at nominal multivariable p value (123 events, N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), fibroblast growth factor 23 (FGF-23), fatty acid-binding protein 4 (FABP4), growth differentiation factor 15 (GDF-15) and interleukin-6 (IL-6)). Of those, NT-pro-BNP and FGF-23 were also associated with AF after adjusting for established AF risk factors. In a prespecified secondary analysis pooling the two data sets, T-cell immunoglobulin and mucin domain 1 (TIM-1) and adrenomedullin (AM) were also significantly related to incident AF in addition to the aforementioned five proteins (Bonferroni-adjustment). The addition of NT-pro-BNP to a model with established risk factors increased the C-statistic from 0.605 to 0.676 (p<0.0001).\n\nUsing a novel proteomics approach, we confirmed the previously reported association between NT-pro-BNP, FGF-23, GDF-15 and incident AF, and also discovered four proteins (FABP4, IL-6, TIM-1 and AM) that could be of importance in the development of AF.", "doi": "10.1136/heartjnl-2016-309764", "pmid": "27609943", "labels": {"Clinical Biomarkers": "Service", "PLA and Single Cell Proteomics": "Service", "Affinity Proteomics Uppsala": "Service"}, "xrefs": [{"db": "pii", "key": "heartjnl-2016-309764"}], "notes": [], "created": "2017-05-03T13:02:17.936Z", "modified": "2023-04-14T13:56:17.464Z"}, {"entity": "publication", "iuid": "2aebfba2d6f7437a881e7bd5a0c8b561", "links": {"self": {"href": "https://publications.scilifelab.se/publication/2aebfba2d6f7437a881e7bd5a0c8b561.json"}, "display": {"href": "https://publications.scilifelab.se/publication/2aebfba2d6f7437a881e7bd5a0c8b561"}}, "title": "The association between plasma homocysteine and coronary heart disease is modified by the MTHFR 677C>T polymorphism.", "authors": [{"family": "Mehlig", "given": "K", "initials": "K"}, {"family": "Leander", "given": "K", "initials": "K"}, {"family": "de Faire", "given": "U", "initials": "U"}, {"family": "Nyberg", "given": "F", "initials": "F"}, {"family": "Berg", "given": "C", "initials": "C"}, {"family": "Rosengren", "given": "A", "initials": "A"}, {"family": "Bj\u00f6rck", "given": "L", "initials": "L"}, {"family": "Zetterberg", "given": "H", "initials": "H"}, {"family": "Blennow", "given": "K", "initials": "K"}, {"family": "Tognon", "given": "G", "initials": "G"}, {"family": "Tor\u00e9n", "given": "K", "initials": "K"}, {"family": "Strandhagen", "given": "E", "initials": "E"}, {"family": "Lissner", "given": "L", "initials": "L"}, {"family": "Thelle", "given": "D", "initials": "D"}], "type": "journal article", "published": "2013-12-00", "journal": {"volume": "99", "issn": "1468-201X", "issue": "23", "pages": "1761-1765", "title": "Heart", "issn-l": "1355-6037"}, "abstract": "An elevated level of total plasma homocysteine (tHcy) has been associated with risk of coronary heart disease (CHD). The level of tHcy is affected by lifestyle, in addition to genetic predisposition. The methylene tetrahydrofolate reductase (MTHFR) 677C>T polymorphism (rs1801133) is among the strongest genetic predictors of tHcy. We examined whether the association between tHcy and CHD is modified by the MTHFR 677C>T polymorphism.\n\nData from two case-control studies of first-time myocardial infarction (MI), Stockholm Heart Epidemiology Programme (SHEEP), and for MI and unstable angina, INTERGENE, were analysed in parallel.\n\nTHcy was determined in a total of 1150 cases and 1753 controls.\n\nNone.\n\nThe outcome comprised first-time MI and unstable angina, subsumed as CHD. Logistic regression was used to investigate the association between tHcy and CHD, and its modification by genotype.\n\nHigh tHcy was confirmed to be a risk factor for CHD in both studies. In SHEEP, the association between tHcy and MI was observed in MTHFR 677 C-homozygotes (OR=1.4, 95% CI 1.2 to 1.6, for a difference by 1 SD of log tHcy) and in heterozygotes (OR=1.3, 95% CI 1.1 to 1.6) but not in T-homozygotes, independent of smoking, physical activity and obesity. An effect modification of similar magnitude was observed but not statistically significant in the smaller INTERGENE study, and confirmed in a meta-analysis of both studies.\n\nTwo Swedish case-control studies showed that the association between elevated tHcy and CHD was confined to carriers of the MTHFR 677 C-allele, which could have implications for the efficiency of tHcy-lowering treatment.", "doi": "10.1136/heartjnl-2013-304460", "pmid": "24014284", "labels": {"Mutation Analysis Facility (MAF)": null}, "xrefs": [{"db": "pii", "key": "heartjnl-2013-304460"}], "notes": [], "created": "2017-05-04T15:03:35.602Z", "modified": "2017-05-30T12:45:38.356Z"}], "created": "2017-05-09T09:12:51.497Z", "modified": "2020-11-27T13:14:03.185Z"}