Katrien De Bock

ORCID: 0000-0001-8232-4663
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About
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Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Muscle Physiology and Disorders
  • Adipose Tissue and Metabolism
  • Angiogenesis and VEGF in Cancer
  • Muscle metabolism and nutrition
  • Mitochondrial Function and Pathology
  • Tissue Engineering and Regenerative Medicine
  • Exercise and Physiological Responses
  • Diet and metabolism studies
  • Metabolism, Diabetes, and Cancer
  • Nutrition and Health in Aging
  • Tendon Structure and Treatment
  • Epigenetics and DNA Methylation
  • Cancer, Lipids, and Metabolism
  • PARP inhibition in cancer therapy
  • Liver Disease Diagnosis and Treatment
  • Veterinary Equine Medical Research
  • Melanoma and MAPK Pathways
  • Autophagy in Disease and Therapy
  • Histone Deacetylase Inhibitors Research
  • Eicosanoids and Hypertension Pharmacology
  • CAR-T cell therapy research
  • Cardiovascular Effects of Exercise
  • MicroRNA in disease regulation
  • Immune cells in cancer

University of Zurich
2024-2025

ETH Zurich
2016-2025

Department of Medical Sciences
2019-2025

Institute for Biomedical Engineering
2024

École Polytechnique Fédérale de Lausanne
2023-2024

Board of the Swiss Federal Institutes of Technology
2020

KU Leuven
2009-2018

VIB-KU Leuven Center for Cancer Biology
2012-2018

Vlaams Instituut voor Biotechnologie
2009-2013

VIB-KU Leuven Center for Microbiology
2010

Abstract mTORC1 is an important regulator of muscle mass but how it modulated by oxygen and nutrients not completely understood. We show that loss the prolyl hydroxylase domain isoform 1 sensor in mice (PHD1 KO ) reduces mass. PHD1 muscles impaired activation response to leucine whereas growth factors or eccentric contractions was preserved. The ability promote activity independent its hydroxylation caused decreased protein content leucyl tRNA synthetase (LRS) sensor. Mechanistically,...

10.1038/s41467-019-13889-6 article EN cc-by Nature Communications 2020-01-10

Endothelial cell (EC)-derived signals contribute to organ regeneration, but angiocrine metabolic communication is not described. We found that EC-specific loss of the glycolytic regulator pfkfb3 reduced ischemic hindlimb revascularization and impaired muscle regeneration. This was caused by ability macrophages adopt a proangiogenic proregenerative M2-like phenotype. Mechanistically, lactate secretion ECs lowered levels in muscle. Addition pfkfb3-deficient restored polarization an...

10.1016/j.cmet.2020.05.004 article EN cc-by-nc-nd Cell Metabolism 2020-06-01

alpha-Actinin-3 is a Z-disc structural protein found only in type II muscle fibers. The X allele of the R577X polymorphism ACTN3 gene results premature stop codon and alpha-actinin-3 deficiency XX homozygotes. Associations between muscle-power performance elite athletes have been described earlier. About 45% fiber proportions are determined by genetic factors. variant could be one contributing genes heritability distribution through its interaction with calcineurin. aim this study was to...

10.1152/physiolgenomics.00173.2007 article EN Physiological Genomics 2007-09-12

Cellular proliferation depends on refilling the tricarboxylic acid (TCA) cycle to support biomass production (anaplerosis). The two major anaplerotic pathways in cells are pyruvate conversion oxaloacetate via carboxylase (PC) and glutamine α-ketoglutarate. Cancers often show an organ-specific reliance either pathway. However, it remains unknown whether they adapt their mode of anaplerosis when metastasizing a distant organ. We measured PC-dependent breast-cancer-derived lung metastases...

10.1016/j.celrep.2016.09.042 article EN cc-by-nc-nd Cell Reports 2016-10-01

Endothelial cells (ECs) are highly glycolytic and generate the majority of their energy via breakdown glucose to lactate. At same time, a main role ECs is allow transport surrounding tissues. GLUT1 (glucose transporter isoform 1/Slc2a1) expressed in central nervous system (CNS) often implicated blood-brain barrier (BBB) dysfunction, but whether how controls EC metabolism function poorly understood.We evaluated endothelial during postnatal CNS development as well at adult BBB.Inhibition...

10.1161/circresaha.119.316463 article EN cc-by-nc-nd Circulation Research 2020-05-14

Abstract A broad range of brain pathologies critically relies on the vasculature, and cerebrovascular disease is a leading cause death worldwide. However, cellular molecular architecture human vasculature remains incompletely understood 1 . Here we performed single-cell RNA sequencing analysis 606,380 freshly isolated endothelial cells, perivascular cells other tissue-derived from 117 samples, 68 fetuses adult patients to construct atlas developing fetal, control diseased vasculature. We...

10.1038/s41586-024-07493-y article EN cc-by Nature 2024-07-10

Tendinopathies are debilitating diseases currently increasing in prevalence and associated costs. There is a need to deepen our understanding of the underlying cell signaling pathways unlock effective treatments. In this work, we screen human tendinopathies find positively enriched IL-6/JAK/STAT alongside signatures populations typically activated by IL-6 other tissues. tendinopathic tendons, also confirm strong presence co-localization IL-6, IL-6R, CD90, an established marker reparative...

10.7554/elife.87092.3 article EN cc-by eLife 2025-02-07

Age-related skeletal muscle sarcopenia is linked with increases in falls, fractures, and death therefore has important socioeconomic consequences. The molecular mechanisms controlling age-related loss humans are not well understood, but likely to involve multiple signaling pathways. This study investigated the regulation of several genes proteins involved activation key pathways promoting hypertrophy, including GH/STAT5, IGF-1/Akt/GSK-3β/4E-BP1, atrophy, TNFα/SOCS-3 Akt/FKHR/atrogene,...

10.1089/rej.2007.0588 article EN Rejuvenation Research 2008-02-01
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