Soluble S. T. 2 Drives Fulminant Myocarditis 02/14/26
Welcome to Cardiology Today â Recorded February 14, 2026. This episode summarizes 5 key cardiology studies on topics like C. C. R. 8 and Left Heart Dysfunction. Key takeaway: Soluble S. T. 2 Drives Fulminant Myocarditis.
Article Links:
Article 1: Elevated Pulmonary Artery Wedge Pressure in Group 1 Pulmonary Hypertension. (Circulation)
Article 2: CCR8 Expression on Regulatory T Cells Reveals Trajectories of Tissue Adaptation and Protects Against Myocardial Infarction-Induced Tissue Damage. (Circulation)
Article 3: Spatial transcriptomics reveals a key role of fibroblast-like vascular smooth muscle cells in human atherosclerotic cell crosstalk and stability. (European heart journal)
Article 4: Soluble ST2 drives fulminant myocarditis progression via the IGF2R-YY1 mitochondrial axis. (European heart journal)
Article 5: Air pollution before and during the COVID-19 pandemic: changes in risk of acute myocardial infarction. (European heart journal)
Full episode page: https://podcast.explainheart.com/podcast/soluble-s-t-2-drives-fulminant-myocarditis-02-14-26/
đ Featured Articles
Article 1: Elevated Pulmonary Artery Wedge Pressure in Group 1 Pulmonary Hypertension.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41685452
Summary: The study identified a distinct subgroup of patients within adjudicated Group 1 Pulmonary Hypertension who demonstrated an elevated pulmonary artery wedge pressure, exceeding 15 mmHg. It characterized this patient population by comparing their profiles to those with normal pulmonary artery wedge pressure and to patients with combined pre- and postcapillary pulmonary hypertension. This work establishes that not all Group 1 Pulmonary Hypertension patients present with the expected normal pulmonary artery wedge pressure, highlighting diagnostic complexities.
Article 2: CCR8 Expression on Regulatory T Cells Reveals Trajectories of Tissue Adaptation and Protects Against Myocardial Infarction-Induced Tissue Damage.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41685444
Summary: C. R. 8 Expression on Regulatory T Cells Reveals Trajectories of Tissue Adaptation and Protects Against Myocardial Infarction-Induced Tissue Damage. This study revealed that C. C. R. 8 expression on regulatory T cells dictates their tissue adaptation trajectories within the heart following myocardial infarction. It found that these C. C. R. 8-positive regulatory T cells provide protection against myocardial infarction-induced tissue damage. The data delineated specific differentiation pathways of heart regulatory T cells in a murine model, establishing a molecular mechanism for regulatory T cell-mediated cardiac protection.
Article 3: Spatial transcriptomics reveals a key role of fibroblast-like vascular smooth muscle cells in human atherosclerotic cell crosstalk and stability.
Journal: European heart journal
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41685669
Summary: This study, using spatial and single-cell transcriptomics on 13 human carotid plaques, revealed a key role for fibroblast-like vascular smooth muscle cells in atherosclerotic cell crosstalk and plaque stability. It precisely mapped intercellular communication patterns within the human plaque microenvironments. The data demonstrated that these specific fibroblast-like vascular smooth muscle cells are critical mediators, identifying specific cellular interactions as potential novel targets for preventing atherosclerotic events.
Article 4: Soluble ST2 drives fulminant myocarditis progression via the IGF2R-YY1 mitochondrial axis.
Journal: European heart journal
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41684269
Summary: T. 2 drives fulminant myocarditis progression via the I. G. F. 2. R. minus Y. Y. 1 mitochondrial axis. This study demonstrated that soluble S. T. 2 drives the progression of fulminant myocarditis via the I. G. F. 2. R. minus Y. Y. 1 mitochondrial axis. It defined the cellular source and function of soluble S. T. 2 in a Coxsackievirus B3-induced fulminant myocarditis mouse model. The research found that markedly elevated soluble S. T. 2 directly contributes to disease pathogenesis, establishing a critical mechanistic pathway that could be targeted for treating this high-mortality inflammatory cardiomyopathy.
Article 5: Air pollution before and during the COVID-19 pandemic: changes in risk of acute myocardial infarction.
Journal: European heart journal
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41684267
Summary: O. V. I. D. minus 19 pandemic: changes in risk of acute myocardial infarction. This study established ambient P. M. 2.5 exposure as a known risk factor for acute myocardial infarction, distinguishing myocardial infarction with non-obstructive coronary arteries as a distinct subtype from myocardial infarction with obstructive coronary disease. It capitalized on the C. O. V. I. D. minus 19 pandemic public health measures, which altered exposure patterns, as a natural experiment. The research characterized the association between short-term P. M. 2.5 exposure and these acute myocardial infarction subtypes during this unique period, providing crucial insights into how environmental shifts can influence risk profiles.
đ Transcript
Today’s date is February 14, 2026. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. Elevated Pulmonary Artery Wedge Pressure in Group 1 Pulmonary Hypertension. The study identified a distinct subgroup of patients within adjudicated Group 1 Pulmonary Hypertension who demonstrated an elevated pulmonary artery wedge pressure, exceeding 15 mmHg. It characterized this patient population by comparing their profiles to those with normal pulmonary artery wedge pressure and to patients with combined pre- and postcapillary pulmonary hypertension. This work establishes that not all Group 1 Pulmonary Hypertension patients present with the expected normal pulmonary artery wedge pressure, highlighting diagnostic complexities.
Article number two. C. C. R. 8 Expression on Regulatory T Cells Reveals Trajectories of Tissue Adaptation and Protects Against Myocardial Infarction-Induced Tissue Damage. This study revealed that C. C. R. 8 expression on regulatory T cells dictates their tissue adaptation trajectories within the heart following myocardial infarction. It found that these C. C. R. 8-positive regulatory T cells provide protection against myocardial infarction-induced tissue damage. The data delineated specific differentiation pathways of heart regulatory T cells in a murine model, establishing a molecular mechanism for regulatory T cell-mediated cardiac protection.
Article number three. Spatial transcriptomics reveals a key role of fibroblast-like vascular smooth muscle cells in human atherosclerotic cell crosstalk and stability. This study, using spatial and single-cell transcriptomics on 13 human carotid plaques, revealed a key role for fibroblast-like vascular smooth muscle cells in atherosclerotic cell crosstalk and plaque stability. It precisely mapped intercellular communication patterns within the human plaque microenvironments. The data demonstrated that these specific fibroblast-like vascular smooth muscle cells are critical mediators, identifying specific cellular interactions as potential novel targets for preventing atherosclerotic events.
Article number four. Soluble S. T. 2 drives fulminant myocarditis progression via the I. G. F. 2. R. minus Y. Y. 1 mitochondrial axis. This study demonstrated that soluble S. T. 2 drives the progression of fulminant myocarditis via the I. G. F. 2. R. minus Y. Y. 1 mitochondrial axis. It defined the cellular source and function of soluble S. T. 2 in a Coxsackievirus B3-induced fulminant myocarditis mouse model. The research found that markedly elevated soluble S. T. 2 directly contributes to disease pathogenesis, establishing a critical mechanistic pathway that could be targeted for treating this high-mortality inflammatory cardiomyopathy.
Article number five. Air pollution before and during the C. O. V. I. D. minus 19 pandemic: changes in risk of acute myocardial infarction. This study established ambient P. M. 2.5 exposure as a known risk factor for acute myocardial infarction, distinguishing myocardial infarction with non-obstructive coronary arteries as a distinct subtype from myocardial infarction with obstructive coronary disease. It capitalized on the C. O. V. I. D. minus 19 pandemic public health measures, which altered exposure patterns, as a natural experiment. The research characterized the association between short-term P. M. 2.5 exposure and these acute myocardial infarction subtypes during this unique period, providing crucial insights into how environmental shifts can influence risk profiles.
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đ Keywords
C. C. R. 8, Left Heart Dysfunction, P. M. 2.5, C. O. V. I. D. minus 19, Coxsackievirus B3, Spatial Transcriptomics, I. G. F. 2. R. minus Y. Y. 1 Axis, Air Pollution, Cell Crosstalk, Atherosclerotic Plaques, Myocardial Infarction, Cardiac Protection, Fibroblast-like Vascular Smooth Muscle Cells, Pulmonary Artery Wedge Pressure, Fulminant Myocarditis, Acute Myocardial Infarction, Tissue Damage, Plaque Stability, Pulmonary Hypertension, Group 1 Pulmonary Hypertension, Regulatory T Cells, Inflammatory Cardiomyopathy, Precapillary Hypertension, Soluble S. T. 2, Myocardial Infarction with Non-obstructive Coronary Arteries.
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