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Erika Gustafsson

Researcher at Lund University

Publications -  46
Citations -  5782

Erika Gustafsson is an academic researcher from Lund University. The author has contributed to research in topics: Perlecan & Extracellular matrix. The author has an hindex of 27, co-authored 46 publications receiving 5365 citations. Previous affiliations of Erika Gustafsson include Uppsala University & Umeå University.

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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

TL;DR: It is shown that cardiac fibrosis is associated with the emergence of fibroblasts originating from endothelial cells, suggesting an endothelial-mesenchymal transition (EndMT) similar to events that occur during formation of the atrioventricular cushion in the embryonic heart.
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Perlecan Maintains the Integrity of Cartilage and Some Basement Membranes

TL;DR: The chondrodysplasia is characterized by a reduction of the fibrillar collagen network, shortened collagen fibers, and elevated expression of cartilage extracellular matrix genes, suggesting that perlecan protects cartilageextracllular matrix from degradation.
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Caspase-8 Serves Both Apoptotic and Nonapoptotic Roles

TL;DR: Caspase-8 deletion in bone-marrow cells resulted in arrest of hemopoietic progenitor functioning, and in cells of the myelomonocytic lineage, its deletion led to arrest of differentiation into macrophages and to cell death.
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Endothelium-specific platelet-derived growth factor-B ablation mimics diabetic retinopathy.

TL;DR: It is reported that endothelium‐restricted ablation of platelet‐derived growth factor‐B generates viable mice with extensive inter‐ and intra‐individual variation in the density of pericytes throughout the CNS, and a strong inverse correlation between pericyte density and the formation of a range of retinal microvascular abnormalities strongly reminiscent of those seen in diabetic humans.
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Endothelium-specific ablation of PDGFB leads to pericyte loss and glomerular, cardiac and placental abnormalities.

TL;DR: The endothelium-restricted Pdgfb knockout mutants survived into adulthood with persistent pathological changes, including brain microhemorrhages, focal astrogliosis, and kidney glomerulus abnormalities, suggesting that they may serve as models for some of the pathogenic events of vascular complications to diabetes.