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P7 Short-term glucocorticoid excess induces cardiac remodelling and changes in cardiac function
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P7 Short-term glucocorticoid excess induces cardiac remodelling and changes in cardiac function
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Journal Article
P7 Short-term glucocorticoid excess induces cardiac remodelling and changes in cardiac function
2025
Overview
Glucocorticoid (GC) treatment is a cornerstone in the management of inflammatory diseases and adrenal insufficiency. Chronic GC exposure increases the risk of cardiovascular disease, with higher incidence of left ventricular hypertrophy and myocardial remodelling. Despite prevalent clinical use, the mechanisms underlying GC-induced cardiac pathology remain poorly understood. Here we aimed to characterise a mouse model of GC excess to investigate the effects on cardiac function and remodelling.Adult (8-week old) male C57Bl/6J mice were adrenalectomised and administered either vehicle (1% ethanol) or corticosterone (100 μg/mL) in drinking water for 4 weeks (n=10 per group). After 4 weeks’ cardiac structure and function were investigated by high-resolution ultrasound. 48 h post-imaging, mice were culled by decapitation and blood and hearts harvested for histological (PSR and WGA) and transcriptomic (bulk RNA-sequencing) analysis. In a small pilot-study, anaesthetised mice (n=1 per group) were injected (IV) with 3.7 MBq [68Ga]-FAPI and PET/CT scans performed to determine extent of cardiac fibrosis.Corticosterone significantly increased ejection fraction and decreased end diastolic volume, with a trend towards increased diastolic ventricular wall thickness (P=0.06) compared to vehicle. Histological analyses revealed increased collagen content (PSR) and increased cardiomyocyte size in hearts of corticosterone-treated mice. Transcriptomic analysis of hearts revealed >2000 differentially expressed genes, and enrichment of pathways relating to extracellular matrix remodelling, consistent with the development of fibrosis. To assess non-invasive evaluation of potential GC-induced cardiac fibrosis, [68Ga]-FAPI uptake was analysed, with increased uptake observed in the heart from corticosterone-, but not vehicle-treated mice.This study demonstrates that GC excess, even at a relatively short duration induces cardiac remodelling, in parallel with changes in cardiac function. Future work will explore the transcriptional basis of this remodelling with the aim of identifying the cellular drivers behind fibrosis, in parallel with facilitating improved diagnostics and targeted therapeutic interventions.
Publisher
BMJ Publishing Group LTD
Subject
