<?xml version='1.0' encoding='utf-8'?>
<?xml-stylesheet type="text/xsl" href="/v2/static/oai2.xsl"?>
<OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd">
  <responseDate>2026-10-09T19:52:52Z</responseDate>
  <request identifier="oai:figshare.com:article/33978007" metadataPrefix="oai_dc" verb="GetRecord">https://api.figshare.com/v2/oai</request>
  <GetRecord>
    <record>
      <header>
        <identifier>oai:figshare.com:article/33978007</identifier>
        <datestamp>2026-09-30T00:26:38Z</datestamp>
        <setSpec>category_24712</setSpec>
        <setSpec>portal_12</setSpec>
        <setSpec>item_type_5</setSpec>
        <setSpec>month_year_09_2026</setSpec>
      </header>
      <metadata>
        <oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"  xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
          <dc:title>Shashika Munasingha: Mitochondria Dysfunction in Diabetic Human Heart Tissue</dc:title>
          <dc:creator>Shashika Munasingha (17069833)</dc:creator>
          <dc:creator>Kenneth Tran (1201914)</dc:creator>
          <dc:creator>Toan Pham (1219026)</dc:creator>
          <dc:creator>Marie-Louise Ward (1207836)</dc:creator>
          <dc:creator>Vijay Rajagopal (791955)</dc:creator>
          <dc:subject>Cell physiology</dc:subject>
          <dc:subject>Diabetes</dc:subject>
          <dc:subject>Mitochondria</dc:subject>
          <dc:subject>Phosphate</dc:subject>
          <dc:subject>Heart</dc:subject>
          <dc:subject>Cardiomyocyte</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;Introduction:&lt;br&gt;Diabetes is a major risk factor for heart failure, with mitochondrial dysfunction contributing to impaired energy production, structural alterations, and dysregulated inorganic phosphate (Pi) metabolism. No previous study has investigated these characteristics together in human cardiac mitochondria.&lt;br&gt;Method:&lt;br&gt;High-resolution fluorespirometry and transmission electron microscopy were used to assess: (i) mitochondrial function at a range of Pi concentrations, and (ii) mitochondrial structure in human right atrial appendage tissue from consenting patients undergoing coronary artery bypass grafting.&lt;br&gt;Conclusion:&lt;br&gt;Results have shown that, no differences were in mitochondrial content and oxygen utilization efficiency for ATP production between groups. However, human cardiac mitochondrial respiration is impaired during active ATP synthesis. Inorganic phosphate regulates mitochondrial respiration at low respiration rates under higher phosphate concentrations in T2D group compared to ND. The higher Pi levels reported in diabetic patients appear to be a compensatory mechanism to maintain mitochondrial respiration.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-30T00:26:38Z</dc:date>
          <dc:type>Image</dc:type>
          <dc:type>Poster</dc:type>
          <dc:identifier>10.17608/k6.auckland.33978007.v2</dc:identifier>
          <dc:relation>https://figshare.com/articles/poster/Mitochondria_Dysfunction_in_Diabetic_Human_Heart_Tissue/33978007</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
        </oai_dc:dc>
      </metadata>
    </record>
  </GetRecord>
</OAI-PMH>
