Helena Idborg

Helena Idborg

Laboratoriesamordnare
E-postadress: helena.idborg@ki.se
Besöksadress: CMM, L8:02, Karolinska Universitetssjukhuset Solna, 17176 Stockholm
Postadress: K2 Medicin, Solna, K2 Reuma Jakobsson P, 171 77 Stockholm
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Artiklar

Alla övriga publikationer

Forskningsbidrag

  • Swedish Research Council
    1 January 2024 - 31 December 2026
    Prostaglandin (PG) E2 is formed from arachidonic acid by the enzymatic actions of either cyclooxygenase (COX)-1 or COX-2 into PGH2, which is further metabolized by microsomal prostaglandin E synthase-1 (mPGES-1) into PGE2. mPGES-1 has emerged as a cardiovascular safe anti-inflammatory drug target. Our characterizations of inhibitors of mPGES-1 demonstrate their potent anti-inflammatory actions while causing relaxation of arteries. mPGES-1 inhibition also significantly protects heart functions following myocardial infarction in vivo. The underlying mechanisms include inhibition of PGE2 biosynthesis, an increase of local prostacyclin formation, no effects on the ADMA-NO pathway and an unbroken formation of anti-inflammatory PGD2/15-deoxy-PGJ2 ( a cyclopentenone). These compounds are considered anti-inflammatory and antiviral and recognized as a part of the family “specialized pro-resolving lipid mediators”. We have identified MGST3 as the key enzyme conjugating cyclopentenone with glutathione. Inhibition of MGST3 leads to increased 15-deoxy-PGJ2 levels with lesser amounts of PGE2. We aim to characterize MGST3 as a novel modulator of inflammation. Furthermore, we will investigate prostaglandins and other lipids as biomarkers for rheumatoid arthritis. We will also characterize our findings demonstrating activation of the thromboxane A2 pathway and platelet activation as a likely mechanism of action for the severe cardiovascular side effects observed for JAK inhibitors.
  • Swedish Research Council
    1 January 2023 - 31 December 2025
    SLE is a heterogeneous autoimmune disease, characterized by the production of autoantibodies. Vascular disease (VD) is a major cause of early morbidity and mortality. Based on clinical experience and unsupervised clustering of 13 clinically relevant autoantibodies in 911 patients, we identified 4 SLE subgroups. Roughly outlined below:Anti-SSA/SSB, skin manifestations, Sjogren’s syndrom, HLA-DRB1*03Anti- dsDNA/nucleosome/Sm, nephritis, enhanced atherosclerosis, early onset, HLA-DRB1*15aPL, clotting disorders, HLA-DRB1*04No autoantibodies, late onset, no HLA association.Aim: To identify mechanisms contributing to autoimmunity and VD, by analyses of the 4 SLE subgroups separately.Method: We have since 1995 followed well-characterized cohorts, comprising &gt
    800 SLE, and 320 controls, every 10 years. Follow-up is ongoing at the clinic and in the National Patient Registries (NPR), where we also identify all Swedish SLE patients (N=7000) and 10 controls/patient.We seek to determine if the 4 groups differ regarding:Proteomics, new autoantibodies and microparticles (vesicles of cellular origin).Blood samples drawn during the different menstrual phases in women with SLE (new approach).Vascular function in the heart, as determined by cardiac magnetic resonance investigation.VD and long-term outcomes in NPRSignificance: Our results can impact how we diagnose and treat SLE in the future. VD mainly affects groups 2 and 3 but by different mechanisms, calling for tailored preventive treatment.
  • Swedish Heart-Lung Foundation
    1 January 2021 - 31 December 2023

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