<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="BioProject" alias="PRJNA773866" accession="SRP342785">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP342785</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA773866</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Epigenetic modulators link mitochondrial redox homoeostasis to cardiac function in a sex-dependent manner (Data set 2)</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>The role of L2-hydroxyglutarate in antioxidative response in heart failure L2HG and D2HG play an important role in maintaining redox homeostasis. As co-factors for TTET1-3, they also influence the epigenomic landscape. To investigate the influence of L2HG and D2HG on cardiomyocyte redox homeostasis, we induced an elevation of L2HG and D2HG in neonatal rat cardiomyocytes (NRCMs) by ShRNA knockdown of L2hgdh and D2hgdh, respectively. In addition, for a more comprehensive examination of their epigenetic impact, we simultaneously elevated L2HG and D2HG while knocking down Tet1-3 in NRCMs using ShRNA targeting of Tet1-3. Subsequently, we extracted RNA and sequenced it following the Smartseq2 protocol.</STUDY_ABSTRACT>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
