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Nuria Barbarroja

Researcher at University of Córdoba (Spain)

Publications -  101
Citations -  3025

Nuria Barbarroja is an academic researcher from University of Córdoba (Spain). The author has contributed to research in topics: Inflammation & Antiphospholipid syndrome. The author has an hindex of 30, co-authored 89 publications receiving 2416 citations. Previous affiliations of Nuria Barbarroja include Carlos III Health Institute & University of Cambridge.

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Differential Lipid Partitioning Between Adipocytes and Tissue Macrophages Modulates Macrophage Lipotoxicity and M2/M1 Polarization in Obese Mice

TL;DR: The data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism and indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization.
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Antiphospholipid antibodies from patients with the antiphospholipid syndrome induce monocyte tissue factor expression through the simultaneous activation of NF‐κB/Rel proteins via the p38 mitogen‐activated protein kinase pathway, and of the MEK‐1/ERK pathway

TL;DR: The results suggest that aPL induces TF expression in monocytes from APS patients by activating, simultaneously and independently, the phosphorylation of MEK-1/ERK proteins, and the p38 MAP kinase-dependent nuclear translocation and activation of NF-kappaB/Rel proteins.
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The obese healthy paradox: is inflammation the answer?

TL;DR: The results support the concept that NIR-MO individuals lack the inflammatory response that characterizes the IR-MO patient and that IL-6, IL-1beta, ERK and NF-kappaB are important effectors that mediate the inflammation effects promoting insulin resistance.
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Vascular endothelial growth factor expression in monocytes from patients with primary antiphospholipid syndrome.

TL;DR: In this paper, the authors analyzed the expression of VEGF and Flt-1 in monocytes of 55 primary antiphospholipid syndrome (APS) patients, and found that the expression was significantly inhibited by the p38 mitogenactivated protein kinase (MAPK) inhibitor SB203580.
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Neutrophils: Novel key players in Rheumatoid Arthritis. Current and future therapeutic targets.

TL;DR: The pathogenic role of neutrophils in RA, the effect of conventional treatments and biologic therapies, and the new, potential targets of neutophil-derived molecules for the treatment of RA are reviewed.