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        <datestamp>2026-10-01T16:32:55Z</datestamp>
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          <dc:title>Investigating the impact of sacubitril/valsartan on cardiac structure, function, and remodelling in the diabetic heart</dc:title>
          <dc:creator>Narainrit Karuna (21369757)</dc:creator>
          <dc:subject>PUREID: 614670934</dc:subject>
          <dc:subject>diabetes mellitus</dc:subject>
          <dc:subject>cardiomyopathy</dc:subject>
          <dc:subject>sacubitril/valsartan</dc:subject>
          <dc:subject>heart failure</dc:subject>
          <dc:subject>diabetic cardiomyopathy</dc:subject>
          <dc:description>Diabetic cardiomyopathy (DbCM), a pre-heart failure (HF) stage, is recognised as a key intermediate stage and determinant for the future development of HF. To date, there are limited therapeutic options for DbCM. Sacubitril/valsartan, an angiotensin receptor neprilysin inhibitor (ARNI), may have therapeutic potential to improve diabetes-induced cardiac abnormalities. This thesis studied the progression pattern of DbCM and potential benefits of sacubitril/valsartan. Plasma neprilysin activity was positively correlated with worsening cardiac function and structure. Sacubitril/valsartan could offer potential therapeutic benefits for preventing DbCM progression by modulating inflammatory responses via modulating interferon regulatory factor 7 (Irf7), thereby improving pro-fibrotic signalling. Furthermore, elevated B cell receptor-associated protein 31 (BAP31) in diabetic patients with pre-HFpEF receiving sacubitril/valsartan may mitigate the pathogenesis of DbCM. In summary, this thesis provides a signature of progression of DbCM and reveals a key driver in DbCM development. Sacubitril/valsartan may serve as therapeutic options in the context of preventing DbCM progression.&lt;br&gt;&lt;br&gt;&lt;i&gt;Thesis is embargoed until 31st December 2029&lt;/i&gt;.&lt;br&gt;&lt;br&gt;&lt;br&gt;</dc:description>
          <dc:date>2026-10-01T16:32:55Z</dc:date>
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          <dc:identifier>10.17034/32640246.v1</dc:identifier>
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          <dc:rights>All Rights Reserved</dc:rights>
          <dc:rights>Open Access after 2029-12-31</dc:rights>
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