- Cancer, Hypoxia, and Metabolism
- Lipid metabolism and disorders
- Adipose Tissue and Metabolism
- Lipid metabolism and biosynthesis
- Angiogenesis and VEGF in Cancer
- Liver Disease Diagnosis and Treatment
- Lymphatic System and Diseases
- Metabolism, Diabetes, and Cancer
- Mitochondrial Function and Pathology
- Diet, Metabolism, and Disease
- Alzheimer's disease research and treatments
- Cardiovascular Disease and Adiposity
- Metabolomics and Mass Spectrometry Studies
- Diet and metabolism studies
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Adipokines, Inflammation, and Metabolic Diseases
- Renal Diseases and Glomerulopathies
- Coronary Interventions and Diagnostics
- Endoplasmic Reticulum Stress and Disease
- Machine Learning in Bioinformatics
- Peroxisome Proliferator-Activated Receptors
- Cancer, Lipids, and Metabolism
- Chronic Kidney Disease and Diabetes
- Congenital heart defects research
- Axon Guidance and Neuronal Signaling
Karolinska Institutet
2009-2024
Ludwig Cancer Research
2009-2010
University of Helsinki
2009
Vlaams Instituut voor Biotechnologie
2009
KU Leuven
2009
Stockholm University
2006
Recently we have identified the novel mitochondrial peptidase responsible for degrading presequences and other short unstructured peptides in mitochondria, presequence peptidase, which named PreP peptidasome. In present study characterized human homologue, hPreP, brain show its capacity to degrade amyloid beta-protein (Abeta). belongs pitrilysin oligopeptidase family M16C containing an inverted zinc-binding motif. We that hPreP is localized matrix. situ immuno-inactivation studies...
Background— New revascularization therapies are urgently needed for patients with severe coronary heart disease who lack conventional treatment options. Methods and Results— We describe a new proangiogenic approach these no-option using adenoviral (Ad) intramyocardial vascular endothelial growth factor (VEGF)-B 186 gene transfer, which induces myocardium-specific angiogenesis arteriogenesis in pigs rabbits. After acute infarction, AdVEGF-B increased blood vessel area, perfusion, ejection...
Hepatic steatosis is a hallmark of non-alcoholic fatty liver disease (NAFLD), common comorbidity in type 2 diabetes mellitus (T2DM). The pathogenesis NAFLD complex and involves the crosstalk between white adipose tissue (WAT). Vascular endothelial growth factor B (VEGF-B) has been shown to control lipid accumulation by regulating transport properties vasculature. role VEGF-B signaling contribution hepatic T2DM currently not understood.C57BL/6 J mice treated with neutralizing antibody against...
Vascular endothelial growth factor (VEGF) B belongs to the VEGF family, but in contrast VEGF-A, VEGF-B does not regulate blood vessel growth. Instead, controls fatty acid (FA) uptake and was identified as a target for treatment of type 2 diabetes. The regulatory mechanisms controlling Vegfb expression have remained unidentified. We show that peroxisome proliferator–activated receptor γ coactivator 1α (PGC-1α) together with estrogen-related α (ERR-α) regulates Vegfb. Mice overexpressing...
The family of vascular endothelial growth factors (VEGF) contains key regulators blood and lymph vessel development, including VEGF-A, -B, -C, -D, placental factor. role VEGF-B during physiological or pathological angiogenesis has not yet been conclusively delineated. Herein, we investigate the function by generation mouse models cancer with transgenic expression homozygous deletion Vegfb.Ectopic in insulin-producing β-cells pancreas did alter abundance architecture islets Langerhans....
A common observation in diabetic kidney disease is lipid accumulation, but the mechanism(s) underlying this pathology unknown. Inhibition of Vascular endothelial growth factor B (VEGF-B) signaling was shown to prevent glomerular accumulation and ameliorated experimental models. Here, we examined biopsies from patients with Type 2 (84 %) 1 diabetes (16 %), combined data mining RNA-seq dataset analyses disease. In glomeruli, mesangial cell-derived VEGF-B expression increased, positively...