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Pharmacological inhibition of 11ßhydroxysteroid dehydrogenase type 1 after myocardial infarction targets extracellular matrix processing and preserves cardiac function in a translational mini-pig model

2024-12-05

Abstract excerpt

<h4>Background and Purpose</h4> Plasma glucocorticoids (GCs) increase acutely after myocardial infarction (MI), thereafter tissue levels are amplified selectively within cells expressing 11ßHydroxysteroid Dehydrogenase type 1 (11ßHSD1) that regenerates active GCs from circulating metabolites. GCs initially protect cardiomyocytes and prevent excessive inflammation after MI but can also suppress subsequent wound re...

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Literature Corpus work
a54bad88-a2d2-5af4-a44d-522e639a5d13
DOI
10.1101/2024.12.02.626322
Open publication

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Pharmacological inhibition of 11ßhydroxysteroid dehydrogenase type 1 after myocardial infarction targets extracellular matrix processing and preserves cardiac function in a translational mini-pig modelDOI 10.1101/2024.12.02.626322
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