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Project
Liver Fibrosis Initiation revisited (FWOAL1046)
Liver fibrosis is the pathological condition of the liver resulting from
sustained wound healing in response to various causes of liver injury,
including chronic alcohol abuse, viral infections or obesity.
Liver disease remains a global issue, with an estimated death toll of
over 1.3 million deaths due to liver cirrhosis, the advanced form of
liver fibrosis. Fibrosis, or scarring of the liver, constitutes the
deposition of excessive amounts of extra-cellular matrix, which is
produced by activated hepatic stellate cells (HSCs) upon liver
damage. Although extensively investigated, the initiating events that
trigger and orchestrate HSC activation are still not entirely
understood. We have evidence that suggests that the processes that
drive HSC activation in a healthy person also play a role in people
suffering from a chronic liver disiease. We also could show that
accessibility to DNA is changed rapidly upon liver injury and believe
that this is instrumental for further activation of these cells . In this
project we will investigate the reorganisation of the DNA and
dynamics of gene transcription during the first days after liver injury
and recovery. The information obtained will allow us to target the key
molecules and process involved in the initiation of fibrosis by using
several complementary in vitro models of liver fibrosis. A detailed
molecular understanding of these first events that drive HSC
activation will fuel novel strategies to treat patients with liver cirrhosis.
sustained wound healing in response to various causes of liver injury,
including chronic alcohol abuse, viral infections or obesity.
Liver disease remains a global issue, with an estimated death toll of
over 1.3 million deaths due to liver cirrhosis, the advanced form of
liver fibrosis. Fibrosis, or scarring of the liver, constitutes the
deposition of excessive amounts of extra-cellular matrix, which is
produced by activated hepatic stellate cells (HSCs) upon liver
damage. Although extensively investigated, the initiating events that
trigger and orchestrate HSC activation are still not entirely
understood. We have evidence that suggests that the processes that
drive HSC activation in a healthy person also play a role in people
suffering from a chronic liver disiease. We also could show that
accessibility to DNA is changed rapidly upon liver injury and believe
that this is instrumental for further activation of these cells . In this
project we will investigate the reorganisation of the DNA and
dynamics of gene transcription during the first days after liver injury
and recovery. The information obtained will allow us to target the key
molecules and process involved in the initiation of fibrosis by using
several complementary in vitro models of liver fibrosis. A detailed
molecular understanding of these first events that drive HSC
activation will fuel novel strategies to treat patients with liver cirrhosis.
Date:1 Jan 2022 → Today
Keywords:Initiation of liver fibrosis, Chromatin structure, Molecular mechanism of hepatic stellate cell activation
Disciplines:Cell physiology, Epigenetics, Hepatology