Key result
Porcine CTEPH model shows RV cardiomyocyte Ca2+ cycling remodeling and altered STIM1L expression.
Why the study?
Pathophysiological mechanisms involved in right ventricular failure remain elusive due to a lack of relevant animal models.
Answers are grounded in this paper and cite their sources.
BACKGROUND: handling, remain elusive due to the lack of relevant animal models. In this study, we aim to understand better the pathophysiological mechanisms involved in RV failure. METHODS: We used the chronic thromboembolic pulmonary hypertension (CTEPH) pig model, which leads to progressive RV hypertrophy and dysfunction. Cellular, molecular unbiased global transcriptional profiling and biochemical analyses were performed on RV cardiomyocytes from CTEPH and Sham-operated pigs. RESULTS: sensor protein STIM1L (stromal interaction molecule 1 long isoform) in CTEPH myocytes as well as in RV from human patients with pulmonary arterial hypertension. CONCLUSIONS: cycling remodeling that participates in the pathogenesis of RV dysfunction and may constitute therapeutic targets to limit the development of RV dysfunction.
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Antigny et al. (2025) studied Right ventricular dysfunction / Chronic thromboembolic pulmonary hypertension. Chronic thromboembolic pulmonary hypertension (CTEPH) model vs. Sham-operated pigs was evaluated on Ca2+ cycling remodeling and STIM1L expression. The CTEPH pig model demonstrated Ca2+ cycling remodeling and altered expression of the sensor protein STIM1L in right ventricular cardiomyocytes, similar to human patients with pulmonary arterial hypertension.
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