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<span class="word">Efficacy <span class="word">of <span class="word"><span class="changedDisabled">Antihypertensive <span class="word"><span class="changedDisabled">Drugs <span class="word">and <span class="word">miR-<span class="word">632 <span class="word"><span class="changedDisabled">Inhibition <span class="word">on <span class="word"><span class="changedDisabled">Parietal <span class="word"><span class="changedDisabled">Remodeling <span class="word">in <span class="word">a <span class="word"><span class="changedDisabled">Model <span class="word">of <span class="word">Marfan <span class="word"><span class="changedDisabled">Thoracic <span class="word"><span class="changedDisabled">Aortic <span class="word"><span class="changedDisabled">Aneurysm

2026-05-13

Abstract excerpt

<h4>Background: </h4> Marfan syndrome (MFS) is a connective tissue disorder caused by FBN1 mutations, leading to elastic fiber disarray and early thoracic aortic aneurysm (TAA) formation. Currently, pharmacological treatments lack specificity and only delay progression. We previously reported a specific TGFβ-driven miR-632 up-regulation in MFS TAA tissues and blood causing smooth muscle cell dedifferentiation and...

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Literature Corpus work: 9d3ebdb8-deba-5290-8f56-fa6858fcf8b7
DOI: 10.20944/preprints202605.0917.v1

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<span class="word">Efficacy <span class="word">of <span class="word"><span class="changedDisabled">Antihypertensive <span class="word"><span class="changedDisabled">Drugs <span class="word">and <span class="word">miR-<span class="word">632 <span class="word"><span class="changedDisabled">Inhibition <span class="word">on <span class="word"><span class="changedDisabled">Parietal <span class="word"><span class="changedDisabled">Remodeling <span class="word">in <span class="word">a <span class="wor…DOI 10.20944/preprints202605.0917.v1Read

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