<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE216326" accession="SRP403933">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP403933</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA892994</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE216326</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>RNA-seq Analysis of Sulodexide- and Vehicle-treated TAA induced Fibrotic Mouse Liver Transcriptomes</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Liver fibrosis is the formation of fibrous scar with the deposition of extracellular matrix (ECM) proteins resulting from persistent liver inflammation and has become a huge global health burden. Sulodexide is a heparinoid compound purified from porcine intestine mucosa, which consists of 80% electrophoretically fast-moving heparin and 20% dermatan sulfate, with endothelium protective function. In this study, we evaluated the therapeutic potential of sulodexide in TAA-induced liver fibrosis model. To determine the mechanism of sulodexide in the treatment of liver fibrosis, we performed high throughput sequencing of mRNA in three groups of liver tissue and identified the protective role of sulodexide on liver sinusoidal endothelial cells. Overall design: To investigate the effect of sulodexide on liver fibrosis, we subjected mice randomly into three groups: the control group, the vehicle-treated TAA group and sulodexide-treated TAA group. Liver fibrosis in the mice was induced by feeding with TAA water (400mg/L) for 16 weeks.The treatment was started on the beginning of 13th week. 4 weeks later, the mice were sacrificed with liver and serum collected.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE216326</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
