METTL14 Inhibits Atherogenesis 03/25/26
Welcome to Cardiology Today – Recorded March 25, 2026. This episode summarizes 5 key cardiology studies on topics like P. P. A. R. minus alpha and left ventricular strain. Key takeaway: METTL14 Inhibits Atherogenesis.
Article Links:
Article 1: Parsimonious echocardiography-based model for predicting long-term all-cause mortality in heart failure with preserved ejection fraction. (Heart (British Cardiac Society))
Article 2: Atorvastatin and left ventricular strain during anthracycline-based chemotherapy. (International journal of cardiology)
Article 3: The inflammation-microvascular axis in prognosis: Integrated FAI and AMR assessment for risk stratification after PCI in NSTEMI patients. (International journal of cardiology)
Article 4: METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs. (Cardiovascular research)
Article 5: THBS4 Regulates Pulmonary Hypertension via TGF-β/SMAD2 Signaling. (Hypertension (Dallas, Tex. : 1979))
Full episode page: https://podcast.explainheart.com/podcast/mettl14-inhibits-atherogenesis-03-25-26/
📚 Featured Articles
Article 1: Parsimonious echocardiography-based model for predicting long-term all-cause mortality in heart failure with preserved ejection fraction.
Journal: Heart (British Cardiac Society)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41876216
Summary: Existing Heart Failure Association Pre-test Assessment, Echocardiography and Natriuretic Peptide, Functional testing, Final Aetiology (H. F. A. minus P. E. F. F.) and Heavy, Hypertensive, Atrial Fibrillation, Pulmonary Hypertension, Elder, Filling Pressure (H. Two F. P. E. F.) scores do not adequately stratify long-term all-cause mortality risk in Heart Failure with Preserved Ejection Fraction (H. F. pEF) patients. To address this identified clinical gap, researchers developed and internally validated a parsimonious echocardiography-based model. This new model was designed to provide improved prediction of long-term all-cause mortality in the H. F. pEF patient population.
Article 2: Atorvastatin and left ventricular strain during anthracycline-based chemotherapy.
Journal: International journal of cardiology
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41875954
Summary: Anthracyclines are associated with impaired Left Ventricular (L. V.) deformation, as measured by global longitudinal strain (G. L. S.) and global circumferential strain (G. C. S.). The S. T. O. P. minus C. A. trial investigated whether atorvastatin attenuates these declines in strain during anthracycline-based chemotherapy. Participants with lymphoma receiving anthracyclines were randomized to either placebo or atorvastatin. The study included 150 patients in the placebo group.
Article 3: The inflammation-microvascular axis in prognosis: Integrated FAI and AMR assessment for risk stratification after PCI in NSTEMI patients.
Journal: International journal of cardiology
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41875953
Summary: Patients with non-S. T. minus segment elevation myocardial infarction (N. S. T. E. M. I.) remain at risk of major adverse cardiovascular events (MACE) despite successful percutaneous coronary intervention (P. C. I.). The combined prognostic value of pericoronary fat attenuation index (F. A. I.), a marker of coronary inflammation from coronary computed tomography angiography (C. C. T. A.), and angiography-derived microcirculatory resistance (A. M. R.), a marker of microvascular dysfunction, is underexplored for these patients. This retrospective cohort study assessed this combined prognostic value for improving risk stratification after P. C. I. in N. S. T. E. M. I. patients.
Article 4: METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41873711
Summary: The study found that M. E. T. T. L. 14 inhibits atherogenesis by epigenetically activating Peroxisome Proliferator-Activated Receptors alpha and gamma (P. P. A. R. minus alpha and P. P. A. R. minus gamma) transcription. This mechanism promotes fatty acid oxidation in Vascular Smooth Muscle Cells (V. S. M. C.s). M. E. T. T. L. 14 therefore plays a crucial role in governing cellular processes that regulate atherosclerosis development.
Article 5: THBS4 Regulates Pulmonary Hypertension via TGF-β/SMAD2 Signaling.
Journal: Hypertension (Dallas, Tex. : 1979)
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41873540
Summary: Thrombospondin-4 (THBS4), an Extracellular Matrix (E. C. M.) glycoprotein, regulates pulmonary vascular remodeling in pulmonary hypertension (P. H.). The study found that T. H. B. S. 4 exerts this regulation via Transforming Growth Factor beta / S. M. A. D. 2 (T. G. F. minus beta / S. M. A. D. 2) signaling. This mechanism contributes to the progressive nature of P. H. marked by pulmonary arterial remodeling and right ventricular dysfunction.
📝 Transcript
Today’s date is March 25, 2026. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. Parsimonious echocardiography-based model for predicting long-term all-cause mortality in heart failure with preserved ejection fraction. Existing Heart Failure Association Pre-test Assessment, Echocardiography and Natriuretic Peptide, Functional testing, Final Aetiology (H. F. A. minus P. E. F. F.) and Heavy, Hypertensive, Atrial Fibrillation, Pulmonary Hypertension, Elder, Filling Pressure (H. Two F. P. E. F.) scores do not adequately stratify long-term all-cause mortality risk in Heart Failure with Preserved Ejection Fraction (H. F. pEF) patients. To address this identified clinical gap, researchers developed and internally validated a parsimonious echocardiography-based model. This new model was designed to provide improved prediction of long-term all-cause mortality in the H. F. pEF patient population.
Article number two. Atorvastatin and left ventricular strain during anthracycline-based chemotherapy. Anthracyclines are associated with impaired Left Ventricular (L. V.) deformation, as measured by global longitudinal strain (G. L. S.) and global circumferential strain (G. C. S.). The S. T. O. P. minus C. A. trial investigated whether atorvastatin attenuates these declines in strain during anthracycline-based chemotherapy. Participants with lymphoma receiving anthracyclines were randomized to either placebo or atorvastatin. The study included 150 patients in the placebo group.
Article number three. The inflammation-microvascular axis in prognosis: Integrated FAI and AMR assessment for risk stratification after PCI in NSTEMI patients. Patients with non-S. T. minus segment elevation myocardial infarction (N. S. T. E. M. I.) remain at risk of major adverse cardiovascular events (MACE) despite successful percutaneous coronary intervention (P. C. I.). The combined prognostic value of pericoronary fat attenuation index (F. A. I.), a marker of coronary inflammation from coronary computed tomography angiography (C. C. T. A.), and angiography-derived microcirculatory resistance (A. M. R.), a marker of microvascular dysfunction, is underexplored for these patients. This retrospective cohort study assessed this combined prognostic value for improving risk stratification after P. C. I. in N. S. T. E. M. I. patients.
Article number four. METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs. The study found that M. E. T. T. L. 14 inhibits atherogenesis by epigenetically activating Peroxisome Proliferator-Activated Receptors alpha and gamma (P. P. A. R. minus alpha and P. P. A. R. minus gamma) transcription. This mechanism promotes fatty acid oxidation in Vascular Smooth Muscle Cells (V. S. M. C.s). M. E. T. T. L. 14 therefore plays a crucial role in governing cellular processes that regulate atherosclerosis development.
Article number five. THBS4 Regulates Pulmonary Hypertension via TGF-β/SMAD2 Signaling. Thrombospondin-4 (THBS4), an Extracellular Matrix (E. C. M.) glycoprotein, regulates pulmonary vascular remodeling in pulmonary hypertension (P. H.). The study found that T. H. B. S. 4 exerts this regulation via Transforming Growth Factor beta / S. M. A. D. 2 (T. G. F. minus beta / S. M. A. D. 2) signaling. This mechanism contributes to the progressive nature of P. H. marked by pulmonary arterial remodeling and right ventricular dysfunction.
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🔍 Keywords
P. P. A. R. minus alpha, left ventricular strain, microcirculatory resistance, pulmonary hypertension, H. F. A. minus P. E. F. F. score, S. M. A. D. 2 signaling, fat attenuation index, anthracycline cardiotoxicity, thrombospondin-4, atherogenesis, echocardiography, P. P. A. R. minus gamma, pulmonary vascular remodeling, major adverse cardiovascular events, T. G. F. minus beta, M. E. T. T. L. 14, heart failure with preserved ejection fraction, mortality risk, atorvastatin, global longitudinal strain, percutaneous coronary intervention, H. Two F. P. E. F. score, vascular smooth muscle cells, non-S. T. minus segment elevation myocardial infarction, global circumferential strain.
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Concise summaries of cardiovascular research for professionals.
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