Association Of Myocardial Strain With Clinical Outcomes In Danon Disease
HFSA ePoster Library. Bui Q. 09/10/21; 343508; 271
Quan Bui
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Abstract
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Introduction: The use of cannabidiol (CBD) as a therapy for an ever-growing number of pathologies has gained acceptance by the medical community. The extensive evidence pointing to CBD as an anti-inflammatory and antioxidant agent suggests its potential to prevent pathological changes in the cardiac tissue associated with heart failure (HF).
Methods: We evaluated the cardioprotective effects of a synthetic formulation of CBD in an angiotensin II (AngII) mouse model of HF. We performed PV-Loops to assess the cardiac function and collected heart tissue to measure fibrosis; molecular markers of pathological remodeling and inflammation were assessed. In isolated cardiomyocytes from HF animals, cell shortening, calcium handling, and mitochondrial function were measured. The antihypertrophic properties of CBD were studied in cultured cardiomyoblasts stimulated with AngII and its implications in oxidative stress and mitochondrial pathways.
Results: CBD treatment significantly prevented cardiac dysfunction and the development of fibrosis, see Fig. 1, and cardiomyocyte hypertrophy. A reduction in the mRNA expression of BNP, TGF-β, collagen-1, IL1β, IL6, and elevation of IL10 and apoptosis and caspase activation was observed compared to untreated HF mice. Improved cellular relaxation and calcium handling were also observed in isolated CBD-treated cardiomyocytes, similar to controls. As observed in the animal model, CBD showed an antihypertrophic effect and pathological remodeling markers similar to controls in cultured cardiomyoblasts. CBD also reduced mitochondrial ROS generation and prevented NF-κβ phosphorylation, limiting mitochondrial calcium uptake by regulating the MCU overexpression observed in angiotensin II groups. Of note, mitochondrial calcium overload triggered by the mitochondrial Na/Ca exchanger blocker resulted in hypertrophy and inflammation regardless of CBD administration.
Conclusion: This study demonstrates the potential cardioprotective effects of CBD as a treatment for HF, as observed in the HF mouse model, which improved cardiac function, reduced its inflammatory state, and prevented the development of hypertrophy and fibrosis in the heart tissue.
Methods: We evaluated the cardioprotective effects of a synthetic formulation of CBD in an angiotensin II (AngII) mouse model of HF. We performed PV-Loops to assess the cardiac function and collected heart tissue to measure fibrosis; molecular markers of pathological remodeling and inflammation were assessed. In isolated cardiomyocytes from HF animals, cell shortening, calcium handling, and mitochondrial function were measured. The antihypertrophic properties of CBD were studied in cultured cardiomyoblasts stimulated with AngII and its implications in oxidative stress and mitochondrial pathways.
Results: CBD treatment significantly prevented cardiac dysfunction and the development of fibrosis, see Fig. 1, and cardiomyocyte hypertrophy. A reduction in the mRNA expression of BNP, TGF-β, collagen-1, IL1β, IL6, and elevation of IL10 and apoptosis and caspase activation was observed compared to untreated HF mice. Improved cellular relaxation and calcium handling were also observed in isolated CBD-treated cardiomyocytes, similar to controls. As observed in the animal model, CBD showed an antihypertrophic effect and pathological remodeling markers similar to controls in cultured cardiomyoblasts. CBD also reduced mitochondrial ROS generation and prevented NF-κβ phosphorylation, limiting mitochondrial calcium uptake by regulating the MCU overexpression observed in angiotensin II groups. Of note, mitochondrial calcium overload triggered by the mitochondrial Na/Ca exchanger blocker resulted in hypertrophy and inflammation regardless of CBD administration.
Conclusion: This study demonstrates the potential cardioprotective effects of CBD as a treatment for HF, as observed in the HF mouse model, which improved cardiac function, reduced its inflammatory state, and prevented the development of hypertrophy and fibrosis in the heart tissue.
Introduction: The use of cannabidiol (CBD) as a therapy for an ever-growing number of pathologies has gained acceptance by the medical community. The extensive evidence pointing to CBD as an anti-inflammatory and antioxidant agent suggests its potential to prevent pathological changes in the cardiac tissue associated with heart failure (HF).
Methods: We evaluated the cardioprotective effects of a synthetic formulation of CBD in an angiotensin II (AngII) mouse model of HF. We performed PV-Loops to assess the cardiac function and collected heart tissue to measure fibrosis; molecular markers of pathological remodeling and inflammation were assessed. In isolated cardiomyocytes from HF animals, cell shortening, calcium handling, and mitochondrial function were measured. The antihypertrophic properties of CBD were studied in cultured cardiomyoblasts stimulated with AngII and its implications in oxidative stress and mitochondrial pathways.
Results: CBD treatment significantly prevented cardiac dysfunction and the development of fibrosis, see Fig. 1, and cardiomyocyte hypertrophy. A reduction in the mRNA expression of BNP, TGF-β, collagen-1, IL1β, IL6, and elevation of IL10 and apoptosis and caspase activation was observed compared to untreated HF mice. Improved cellular relaxation and calcium handling were also observed in isolated CBD-treated cardiomyocytes, similar to controls. As observed in the animal model, CBD showed an antihypertrophic effect and pathological remodeling markers similar to controls in cultured cardiomyoblasts. CBD also reduced mitochondrial ROS generation and prevented NF-κβ phosphorylation, limiting mitochondrial calcium uptake by regulating the MCU overexpression observed in angiotensin II groups. Of note, mitochondrial calcium overload triggered by the mitochondrial Na/Ca exchanger blocker resulted in hypertrophy and inflammation regardless of CBD administration.
Conclusion: This study demonstrates the potential cardioprotective effects of CBD as a treatment for HF, as observed in the HF mouse model, which improved cardiac function, reduced its inflammatory state, and prevented the development of hypertrophy and fibrosis in the heart tissue.
Methods: We evaluated the cardioprotective effects of a synthetic formulation of CBD in an angiotensin II (AngII) mouse model of HF. We performed PV-Loops to assess the cardiac function and collected heart tissue to measure fibrosis; molecular markers of pathological remodeling and inflammation were assessed. In isolated cardiomyocytes from HF animals, cell shortening, calcium handling, and mitochondrial function were measured. The antihypertrophic properties of CBD were studied in cultured cardiomyoblasts stimulated with AngII and its implications in oxidative stress and mitochondrial pathways.
Results: CBD treatment significantly prevented cardiac dysfunction and the development of fibrosis, see Fig. 1, and cardiomyocyte hypertrophy. A reduction in the mRNA expression of BNP, TGF-β, collagen-1, IL1β, IL6, and elevation of IL10 and apoptosis and caspase activation was observed compared to untreated HF mice. Improved cellular relaxation and calcium handling were also observed in isolated CBD-treated cardiomyocytes, similar to controls. As observed in the animal model, CBD showed an antihypertrophic effect and pathological remodeling markers similar to controls in cultured cardiomyoblasts. CBD also reduced mitochondrial ROS generation and prevented NF-κβ phosphorylation, limiting mitochondrial calcium uptake by regulating the MCU overexpression observed in angiotensin II groups. Of note, mitochondrial calcium overload triggered by the mitochondrial Na/Ca exchanger blocker resulted in hypertrophy and inflammation regardless of CBD administration.
Conclusion: This study demonstrates the potential cardioprotective effects of CBD as a treatment for HF, as observed in the HF mouse model, which improved cardiac function, reduced its inflammatory state, and prevented the development of hypertrophy and fibrosis in the heart tissue.
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