• Home Dutch
  •  EN 
  • Employee login

Liver fibrosis and hibernation

Title:  Liver fibrosis and hibernation.
Investigator:  EM Verhaag
Promotor:  KN Faber, H Moshage, RH Henning
Summary:  Liver fibrosis is a common feature of chronic liver diseases, and results from continuous or repetitive liver injury. Hepatocyte damage, in the presence of a persistent inflammatory response, activates hepatic stellate cells and portal myofibroblasts, the most important cell types involved in the production of extracellular matrix components. These activated matrix-producing cells drive fibrogenesis. From a clinical point of view, resolution of fibrosis is the ideal strategy to limit or even reverse fibrogenesis and prevent end-stage cirrhosis. Here, we aim to investigate a natural model of effective reversal of tissue fibrosis, i.e. the hibernating Syrian hamsters. Despite the fact that hibernators undergo repetitive cycles of hypothermia (torpor) and rewarming (arousal) during the hibernating season, apparent organ damage is absent. Interestingly, Syrian hamsters develop lung fibrosis during torpor, which is rapidly resolved during the next arousal bout. The aim of the current research is to study liver fibrosis in hibernating Syrian hamsters to identify mechanisms that prevent and/or reverse liver injury and fibrosis, with a special interest in the role of the (innate) immune system.
Financing:  TopMaster bursary
Start:  1-05-2011


Organ damage and the role of CBS in hibernation.
Mechanisms and modulation of the immune response in sterile sepsis.
The CBS/H2S pathway in the brain.
Platelet dynamics in natural and pharmacologically induced hibernation.
Liver fibrosis and hibernation.
Towards prevention of neuroinflammation in major surgery.
Limiting the impact of stroke.
Identification of kinomic key proteins involved in tachycardia and stretch induced cardiomyocyte remodeling.
Role of epigenetic regulation by histone acetylation in the induction of Atrial Fibrillation.
Reversal of cardiomyocyte remodeling in Atrial Fibrillation; the role of protein degradation and translation modulators.
REVersal of cardiomyocyte structural remodeling and Improvement of functional recoVEry in Atrial Fibrillation: REVIVE.
HSF1 Activators Lower cardiomyocyte damage: towards a novel Therapeutic approach to REVERSE Atrial Fibrillation. HALT&REVERSE
Mutations in HSPB5, HSPB7 and BAG3 lead to juvenile DCM.
New therapeutic targets in diabetic kidney disease. A role of GDF-15?
Role of cyclooxygenase signalling on vascular dysfunction in the metabolic syndrome.
Vascular (Dys-)Function as a Determinant of Susceptibility to Diabetic Nephropathy: a Focus on Myogenic Constriction.