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Listen "AI Boosts C. T. A. Heart Risk Prediction. 11/23/25"
Episode Synopsis
Welcome to Cardiology Today – Recorded November 23, 2025. This episode summarizes 5 key cardiology studies on topics like machine learning and C. T. A.. Key takeaway: AI Boosts C. T. A. Heart Risk Prediction..
Article Links:
Article 1: In vitro approaches to mimic cardiac mechanical load dynamics for enhancing maturation and disease modelling. (Cardiovascular research)
Article 2: S1PR1-MYPT1 Maintains Coronary Endothelial Barrier in Pressure-Overloaded Hearts. (Hypertension (Dallas, Tex. : 1979))
Article 3: Nobiletin Prevents Cardiac Hypertrophy via SIRT5-Mediated Downregulation of p300. (Hypertension (Dallas, Tex. : 1979))
Article 4: Primary Aldosteronism: Small Molecule Antagonists of Mutant KCNJ5 Potassium Channels. (Hypertension (Dallas, Tex. : 1979))
Article 5: Machine Learning Model for Atherosclerosis Evaluation and Cardiovascular Risk Prediction Based on Coronary CT Angiography-Analysis From the CREATION Registry. (Circulation. Cardiovascular imaging)
Full episode page: https://podcast.explainheart.com/podcast/ai-boosts-c-t-a-heart-risk-prediction-11-23-25/
Featured Articles
Article 1: In vitro approaches to mimic cardiac mechanical load dynamics for enhancing maturation and disease modelling.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41261979
Summary: Human pluripotent stem cell derived cardiomyocytes hold significant promise for in vitro models of the human heart. Achieving full maturation of these cells requires replicating the native cardiac environment, specifically incorporating active mechanical loads such as preload and afterload. These mechanical cues are essential for enhancing cardiomyocyte maturation and improving the utility of these models for disease modeling. This approach represents a critical strategy for advancing the development of more physiologically relevant human heart models.
Article 2: S1PR1-MYPT1 Maintains Coronary Endothelial Barrier in Pressure-Overloaded Hearts.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41268665
Summary: This study found that coronary microvascular hyperpermeability and subsequent inflammation infiltration are key early characteristics of pressure overload-induced myocardial injury. In mice, endothelial-specific deletion of sphingosine-1-phosphate receptor type one (S1PR1) led to severe pressure overload-induced cardiac dysfunction, while S1PR1 overexpression preserved cardiac function. Researchers demonstrated that S1PR1 activation maintained the coronary endothelial barrier by preventing myosin phosphatase target subunit one (MYPT1) ubiquitination and degradation during pressure overload. These findings reveal a critical role for the S1PR1-MYPT1 pathway in preserving coronary endothelial barrier function and cardiac function under pressure overload, identifying S1PR1 as a potential therapeutic target.
Article 3: Nobiletin Prevents Cardiac Hypertrophy via SIRT5-Mediated Downregulation of p300.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41268664
Summary: This study found that nobiletin treatment attenuated cardiac hypertrophy and improved systolic dysfunction in mice models of transverse aortic constriction. Nobiletin also improved the survival rate of these mice. Mechanistically, nobiletin significantly downregulated E one A binding protein P300 expression by directly binding to and activating Sirtuin 5, which in turn promoted P300 degradation. These findings identify nobiletin as a potent activator of Sirtuin 5, suggesting its potential as a promising therapeutic agent for heart failure.
Article 4: Primary Aldosteronism: Small Molecule Antagonists of Mutant KCNJ5 Potassium Channels.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41263073
Summary: Mutations in the potassium inwardly rectifying channel subfamily J member five (KCNJ5) gene drive aldosterone overproduction in a subset of aldosterone-producing adenomas and familial hyperaldosteronism type three. Researchers identified small molecule compounds that specifically antagonize mutant KCNJ5 channels. Compound three demonstrated specific antagonism of mutant KCNJ5 channels with an inhibitory concentration fifty of 20 nanomolar in electrophysiological studies, showing no activity against wild-type KCNJ5. This compound also inhibited mutant KCNJ5-dependent aldosterone production in human adrenal carcinoma cells, identifying a potent and specific antagonist and a promising therapeutic strategy for primary aldosteronism.
Article 5: Machine Learning Model for Atherosclerosis Evaluation and Cardiovascular Risk Prediction Based on Coronary CT Angiography-Analysis From the CREATION Registry.
Journal: Circulation. Cardiovascular imaging
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41268668
Summary: Machine learning models based on coronary computed tomography angiography (C. T. A.) features demonstrated superior performance in predicting major adverse cardiac events compared to traditional risk factors and the coronary artery calcium score. The XGBoost model achieved the highest predictive power with an area under the curve of 0.887 for five-year major adverse cardiac event prediction. This model showed a hazard ratio of 1.95 with a 95 percent confidence interval of 1.77 to 2.15 for major adverse cardiac events. These findings demonstrate the strong potential of machine learning combined with coronary C. T. A. for personalized atherosclerosis evaluation and cardiovascular risk prediction.
Transcript
Today’s date is November 23, 2025. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. In vitro approaches to mimic cardiac mechanical load dynamics for enhancing maturation and disease modelling. Human pluripotent stem cell derived cardiomyocytes hold significant promise for in vitro models of the human heart. Achieving full maturation of these cells requires replicating the native cardiac environment, specifically incorporating active mechanical loads such as preload and afterload. These mechanical cues are essential for enhancing cardiomyocyte maturation and improving the utility of these models for disease modeling. This approach represents a critical strategy for advancing the development of more physiologically relevant human heart models.
Article number two. S1PR1-MYPT1 Maintains Coronary Endothelial Barrier in Pressure-Overloaded Hearts. This study found that coronary microvascular hyperpermeability and subsequent inflammation infiltration are key early characteristics of pressure overload-induced myocardial injury. In mice, endothelial-specific deletion of sphingosine-1-phosphate receptor type one (S1PR1) led to severe pressure overload-induced cardiac dysfunction, while S1PR1 overexpression preserved cardiac function. Researchers demonstrated that S1PR1 activation maintained the coronary endothelial barrier by preventing myosin phosphatase target subunit one (MYPT1) ubiquitination and degradation during pressure overload. These findings reveal a critical role for the S1PR1-MYPT1 pathway in preserving coronary endothelial barrier function and cardiac function under pressure overload, identifying S1PR1 as a potential therapeutic target.
Article number three. Nobiletin Prevents Cardiac Hypertrophy via SIRT5-Mediated Downregulation of p300. This study found that nobiletin treatment attenuated cardiac hypertrophy and improved systolic dysfunction in mice models of transverse aortic constriction. Nobiletin also improved the survival rate of these mice. Mechanistically, nobiletin significantly downregulated E one A binding protein P300 expression by directly binding to and activating Sirtuin 5, which in turn promoted P300 degradation. These findings identify nobiletin as a potent activator of Sirtuin 5, suggesting its potential as a promising therapeutic agent for heart failure.
Article number four. Primary Aldosteronism: Small Molecule Antagonists of Mutant KCNJ5 Potassium Channels. Mutations in the potassium inwardly rectifying channel subfamily J member five (KCNJ5) gene drive aldosterone overproduction in a subset of aldosterone-producing adenomas and familial hyperaldosteronism type three. Researchers identified small molecule compounds that specifically antagonize mutant KCNJ5 channels. Compound three demonstrated specific antagonism of mutant KCNJ5 channels with an inhibitory concentration fifty of 20 nanomolar in electrophysiological studies, showing no activity against wild-type KCNJ5. This compound also inhibited mutant KCNJ5-dependent aldosterone production in human adrenal carcinoma cells, identifying a potent and specific antagonist and a promising therapeutic strategy for primary aldosteronism.
Article number five. Machine Learning Model for Atherosclerosis Evaluation and Cardiovascular Risk Prediction Based on Coronary CT Angiography-Analysis From the CREATION Registry. Machine learning models based on coronary computed tomography angiography (C. T. A.) features demonstrated superior performance in predicting major adverse cardiac events compared to traditional risk factors and the coronary artery calcium score. The XGBoost model achieved the highest predictive power with an area under the curve of 0.887 for five-year major adverse cardiac event prediction. This model showed a hazard ratio of 1.95 with a 95 percent confidence interval of 1.77 to 2.15 for major adverse cardiac events. These findings demonstrate the strong potential of machine learning combined with coronary C. T. A. for personalized atherosclerosis evaluation and cardiovascular risk prediction.
Thank you for listening. Don’t forget to subscribe.
Keywords
machine learning, C. T. A., primary aldosteronism, familial hyperaldosteronism type three, MYPT1, XGBoost, S1PR1, atherosclerosis, heart failure, major adverse cardiac events, KCNJ5, cardiac tissue engineering, potassium inwardly rectifying channel subfamily J member five, E one A binding protein P300, cardiac hypertrophy, mechanical load, SIRT5, cardiomyocytes, nobiletin, human pluripotent stem cells, cardiac dysfunction, pressure overload, in vitro models, coronary endothelial barrier, aldosterone-producing adenomas, coronary computed tomography angiography, small molecule antagonist, sphingosine-1-phosphate receptor type one, cardiovascular risk prediction, p300, Sirtuin 5, systolic dysfunction, myosin phosphatase target subunit one.
About
Concise summaries of cardiovascular research for professionals.
Subscribe • Share • FollowThe post AI Boosts C. T. A. Heart Risk Prediction. 11/23/25 first appeared on Cardiology Today.
Article Links:
Article 1: In vitro approaches to mimic cardiac mechanical load dynamics for enhancing maturation and disease modelling. (Cardiovascular research)
Article 2: S1PR1-MYPT1 Maintains Coronary Endothelial Barrier in Pressure-Overloaded Hearts. (Hypertension (Dallas, Tex. : 1979))
Article 3: Nobiletin Prevents Cardiac Hypertrophy via SIRT5-Mediated Downregulation of p300. (Hypertension (Dallas, Tex. : 1979))
Article 4: Primary Aldosteronism: Small Molecule Antagonists of Mutant KCNJ5 Potassium Channels. (Hypertension (Dallas, Tex. : 1979))
Article 5: Machine Learning Model for Atherosclerosis Evaluation and Cardiovascular Risk Prediction Based on Coronary CT Angiography-Analysis From the CREATION Registry. (Circulation. Cardiovascular imaging)
Full episode page: https://podcast.explainheart.com/podcast/ai-boosts-c-t-a-heart-risk-prediction-11-23-25/
Featured Articles
Article 1: In vitro approaches to mimic cardiac mechanical load dynamics for enhancing maturation and disease modelling.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41261979
Summary: Human pluripotent stem cell derived cardiomyocytes hold significant promise for in vitro models of the human heart. Achieving full maturation of these cells requires replicating the native cardiac environment, specifically incorporating active mechanical loads such as preload and afterload. These mechanical cues are essential for enhancing cardiomyocyte maturation and improving the utility of these models for disease modeling. This approach represents a critical strategy for advancing the development of more physiologically relevant human heart models.
Article 2: S1PR1-MYPT1 Maintains Coronary Endothelial Barrier in Pressure-Overloaded Hearts.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41268665
Summary: This study found that coronary microvascular hyperpermeability and subsequent inflammation infiltration are key early characteristics of pressure overload-induced myocardial injury. In mice, endothelial-specific deletion of sphingosine-1-phosphate receptor type one (S1PR1) led to severe pressure overload-induced cardiac dysfunction, while S1PR1 overexpression preserved cardiac function. Researchers demonstrated that S1PR1 activation maintained the coronary endothelial barrier by preventing myosin phosphatase target subunit one (MYPT1) ubiquitination and degradation during pressure overload. These findings reveal a critical role for the S1PR1-MYPT1 pathway in preserving coronary endothelial barrier function and cardiac function under pressure overload, identifying S1PR1 as a potential therapeutic target.
Article 3: Nobiletin Prevents Cardiac Hypertrophy via SIRT5-Mediated Downregulation of p300.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41268664
Summary: This study found that nobiletin treatment attenuated cardiac hypertrophy and improved systolic dysfunction in mice models of transverse aortic constriction. Nobiletin also improved the survival rate of these mice. Mechanistically, nobiletin significantly downregulated E one A binding protein P300 expression by directly binding to and activating Sirtuin 5, which in turn promoted P300 degradation. These findings identify nobiletin as a potent activator of Sirtuin 5, suggesting its potential as a promising therapeutic agent for heart failure.
Article 4: Primary Aldosteronism: Small Molecule Antagonists of Mutant KCNJ5 Potassium Channels.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41263073
Summary: Mutations in the potassium inwardly rectifying channel subfamily J member five (KCNJ5) gene drive aldosterone overproduction in a subset of aldosterone-producing adenomas and familial hyperaldosteronism type three. Researchers identified small molecule compounds that specifically antagonize mutant KCNJ5 channels. Compound three demonstrated specific antagonism of mutant KCNJ5 channels with an inhibitory concentration fifty of 20 nanomolar in electrophysiological studies, showing no activity against wild-type KCNJ5. This compound also inhibited mutant KCNJ5-dependent aldosterone production in human adrenal carcinoma cells, identifying a potent and specific antagonist and a promising therapeutic strategy for primary aldosteronism.
Article 5: Machine Learning Model for Atherosclerosis Evaluation and Cardiovascular Risk Prediction Based on Coronary CT Angiography-Analysis From the CREATION Registry.
Journal: Circulation. Cardiovascular imaging
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41268668
Summary: Machine learning models based on coronary computed tomography angiography (C. T. A.) features demonstrated superior performance in predicting major adverse cardiac events compared to traditional risk factors and the coronary artery calcium score. The XGBoost model achieved the highest predictive power with an area under the curve of 0.887 for five-year major adverse cardiac event prediction. This model showed a hazard ratio of 1.95 with a 95 percent confidence interval of 1.77 to 2.15 for major adverse cardiac events. These findings demonstrate the strong potential of machine learning combined with coronary C. T. A. for personalized atherosclerosis evaluation and cardiovascular risk prediction.
Transcript
Today’s date is November 23, 2025. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. In vitro approaches to mimic cardiac mechanical load dynamics for enhancing maturation and disease modelling. Human pluripotent stem cell derived cardiomyocytes hold significant promise for in vitro models of the human heart. Achieving full maturation of these cells requires replicating the native cardiac environment, specifically incorporating active mechanical loads such as preload and afterload. These mechanical cues are essential for enhancing cardiomyocyte maturation and improving the utility of these models for disease modeling. This approach represents a critical strategy for advancing the development of more physiologically relevant human heart models.
Article number two. S1PR1-MYPT1 Maintains Coronary Endothelial Barrier in Pressure-Overloaded Hearts. This study found that coronary microvascular hyperpermeability and subsequent inflammation infiltration are key early characteristics of pressure overload-induced myocardial injury. In mice, endothelial-specific deletion of sphingosine-1-phosphate receptor type one (S1PR1) led to severe pressure overload-induced cardiac dysfunction, while S1PR1 overexpression preserved cardiac function. Researchers demonstrated that S1PR1 activation maintained the coronary endothelial barrier by preventing myosin phosphatase target subunit one (MYPT1) ubiquitination and degradation during pressure overload. These findings reveal a critical role for the S1PR1-MYPT1 pathway in preserving coronary endothelial barrier function and cardiac function under pressure overload, identifying S1PR1 as a potential therapeutic target.
Article number three. Nobiletin Prevents Cardiac Hypertrophy via SIRT5-Mediated Downregulation of p300. This study found that nobiletin treatment attenuated cardiac hypertrophy and improved systolic dysfunction in mice models of transverse aortic constriction. Nobiletin also improved the survival rate of these mice. Mechanistically, nobiletin significantly downregulated E one A binding protein P300 expression by directly binding to and activating Sirtuin 5, which in turn promoted P300 degradation. These findings identify nobiletin as a potent activator of Sirtuin 5, suggesting its potential as a promising therapeutic agent for heart failure.
Article number four. Primary Aldosteronism: Small Molecule Antagonists of Mutant KCNJ5 Potassium Channels. Mutations in the potassium inwardly rectifying channel subfamily J member five (KCNJ5) gene drive aldosterone overproduction in a subset of aldosterone-producing adenomas and familial hyperaldosteronism type three. Researchers identified small molecule compounds that specifically antagonize mutant KCNJ5 channels. Compound three demonstrated specific antagonism of mutant KCNJ5 channels with an inhibitory concentration fifty of 20 nanomolar in electrophysiological studies, showing no activity against wild-type KCNJ5. This compound also inhibited mutant KCNJ5-dependent aldosterone production in human adrenal carcinoma cells, identifying a potent and specific antagonist and a promising therapeutic strategy for primary aldosteronism.
Article number five. Machine Learning Model for Atherosclerosis Evaluation and Cardiovascular Risk Prediction Based on Coronary CT Angiography-Analysis From the CREATION Registry. Machine learning models based on coronary computed tomography angiography (C. T. A.) features demonstrated superior performance in predicting major adverse cardiac events compared to traditional risk factors and the coronary artery calcium score. The XGBoost model achieved the highest predictive power with an area under the curve of 0.887 for five-year major adverse cardiac event prediction. This model showed a hazard ratio of 1.95 with a 95 percent confidence interval of 1.77 to 2.15 for major adverse cardiac events. These findings demonstrate the strong potential of machine learning combined with coronary C. T. A. for personalized atherosclerosis evaluation and cardiovascular risk prediction.
Thank you for listening. Don’t forget to subscribe.
Keywords
machine learning, C. T. A., primary aldosteronism, familial hyperaldosteronism type three, MYPT1, XGBoost, S1PR1, atherosclerosis, heart failure, major adverse cardiac events, KCNJ5, cardiac tissue engineering, potassium inwardly rectifying channel subfamily J member five, E one A binding protein P300, cardiac hypertrophy, mechanical load, SIRT5, cardiomyocytes, nobiletin, human pluripotent stem cells, cardiac dysfunction, pressure overload, in vitro models, coronary endothelial barrier, aldosterone-producing adenomas, coronary computed tomography angiography, small molecule antagonist, sphingosine-1-phosphate receptor type one, cardiovascular risk prediction, p300, Sirtuin 5, systolic dysfunction, myosin phosphatase target subunit one.
About
Concise summaries of cardiovascular research for professionals.
Subscribe • Share • FollowThe post AI Boosts C. T. A. Heart Risk Prediction. 11/23/25 first appeared on Cardiology Today.
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