Welcome to Cardiology Today – Recorded November 23, 2025. This episode summarizes 5 key cardiology studies on topics like cardiovascular disease and lineage differentiation. Key takeaway: BMAL1 Insufficiency Raises Aortic Dissection Risk.
Article Links:
Article 1: Loss of GPR146 decreases plasma levels of HDL cholesterol via post-translational upregulation of SR-B1 protein levels. (Cardiovascular research)
Article 2: BMAL1 insufficiency increases the risk of thoracic aortic aneurysm and dissection. (Cardiovascular research)
Article 3: ChemR23 prevents phenotypic switching of vascular smooth muscle cells into macrophage like foam cells in atherosclerosis. (Cardiovascular research)
Article 4: Advances in single-cell transcriptomics: unraveling the pathogenesis of calcific aortic valve disease. (Cardiovascular research)
Article 5: Transcription regulation by TBX18 in smooth muscle cells is essential for normal aortic development and homeostasis. (Cardiovascular research)
Full episode page: https://podcast.explainheart.com/podcast/bmal1-insufficiency-raises-aortic-dissection-risk-11-23-25/
Featured Articles
Article 1: Loss of GPR146 decreases plasma levels of HDL cholesterol via post-translational upregulation of SR-B1 protein levels.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41271608
Summary: Reduced G-protein coupled receptor 146 (GPR146) expression in humans is associated with decreased levels of both low-density lipoprotein and high-density lipoprotein cholesterol. While GPR146 effects on low-density lipoprotein cholesterol involve the E. R. K. /S. R. E. B. P. 2 pathway, this study found the mechanism for high-density lipoprotein cholesterol reduction involves post-translational upregulation of S. R. minus B. 1 protein levels. This provides a direct mechanistic link for GPR146’s role in high-density lipoprotein metabolism.
Article 2: BMAL1 insufficiency increases the risk of thoracic aortic aneurysm and dissection.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41270048
Summary: This study found that B. M. A. L. 1 insufficiency increases the risk of thoracic aortic aneurysm and dissection. Vascular smooth muscle cell apoptosis plays a key role in this lethal cardiovascular disease, which has high mortality rates and limited pharmacological therapy. The data established a direct link between insufficient B. M. A. L. 1 and increased susceptibility to thoracic aortic aneurysm and dissection by aggravating vascular smooth muscle cell apoptosis.
Article 3: ChemR23 prevents phenotypic switching of vascular smooth muscle cells into macrophage like foam cells in atherosclerosis.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41264461
Summary: This study found that ChemR23 prevents the phenotypic switching of vascular smooth muscle cells into macrophage-like foam cells in atherosclerosis. Previous findings demonstrated that hematopoietic ChemR23 deficiency reduced atherosclerotic lesions by increasing M two macrophages. The current data specify a critical cell-specific function for ChemR23 by inhibiting this harmful transformation of vascular smooth muscle cells directly contributing to atherosclerosis development.
Article 4: Advances in single-cell transcriptomics: unraveling the pathogenesis of calcific aortic valve disease.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41264422
Summary: Single-cell R. N. A. sequencing has revolutionized the study of calcific aortic valve disease. This advanced technique dissects cellular heterogeneity, lineage differentiation, and intercellular crosstalk with unprecedented resolution, revealing novel mechanisms of disease. It also identified new putative therapeutic targets for calcific aortic valve disease, providing a state-of-the-art overview of applications in this research area.
Article 5: Transcription regulation by TBX18 in smooth muscle cells is essential for normal aortic development and homeostasis.
Journal: Cardiovascular research
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/41263385
Summary: This study found that transcription regulation by T. B. X. 18 in smooth muscle cells is essential for normal aortic development and homeostasis. Histological analyses revealed specific T. B. X. 18 expression in smooth muscle cells of both adult and embryonic aortas. The data demonstrated a critical role for T. B. X. 18 in maintaining the integrity and proper formation of this major artery throughout development and into adulthood.
Transcript

Today’s date is November 23, 2025. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. Loss of GPR146 decreases plasma levels of HDL cholesterol via post-translational upregulation of SR-B1 protein levels. Reduced G-protein coupled receptor 146 (GPR146) expression in humans is associated with decreased levels of both low-density lipoprotein and high-density lipoprotein cholesterol. While GPR146 effects on low-density lipoprotein cholesterol involve the E. R. K. /S. R. E. B. P. 2 pathway, this study found the mechanism for high-density lipoprotein cholesterol reduction involves post-translational upregulation of S. R. minus B. 1 protein levels. This provides a direct mechanistic link for GPR146’s role in high-density lipoprotein metabolism.
Article number two. BMAL1 insufficiency increases the risk of thoracic aortic aneurysm and dissection. This study found that B. M. A. L. 1 insufficiency increases the risk of thoracic aortic aneurysm and dissection. Vascular smooth muscle cell apoptosis plays a key role in this lethal cardiovascular disease, which has high mortality rates and limited pharmacological therapy. The data established a direct link between insufficient B. M. A. L. 1 and increased susceptibility to thoracic aortic aneurysm and dissection by aggravating vascular smooth muscle cell apoptosis.
Article number three. ChemR23 prevents phenotypic switching of vascular smooth muscle cells into macrophage like foam cells in atherosclerosis. This study found that ChemR23 prevents the phenotypic switching of vascular smooth muscle cells into macrophage-like foam cells in atherosclerosis. Previous findings demonstrated that hematopoietic ChemR23 deficiency reduced atherosclerotic lesions by increasing M two macrophages. The current data specify a critical cell-specific function for ChemR23 by inhibiting this harmful transformation of vascular smooth muscle cells directly contributing to atherosclerosis development.
Article number four. Advances in single-cell transcriptomics: unraveling the pathogenesis of calcific aortic valve disease. Single-cell R. N. A. sequencing has revolutionized the study of calcific aortic valve disease. This advanced technique dissects cellular heterogeneity, lineage differentiation, and intercellular crosstalk with unprecedented resolution, revealing novel mechanisms of disease. It also identified new putative therapeutic targets for calcific aortic valve disease, providing a state-of-the-art overview of applications in this research area.
Article number five. Transcription regulation by TBX18 in smooth muscle cells is essential for normal aortic development and homeostasis. This study found that transcription regulation by T. B. X. 18 in smooth muscle cells is essential for normal aortic development and homeostasis. Histological analyses revealed specific T. B. X. 18 expression in smooth muscle cells of both adult and embryonic aortas. The data demonstrated a critical role for T. B. X. 18 in maintaining the integrity and proper formation of this major artery throughout development and into adulthood.
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Keywords
cardiovascular disease, lineage differentiation, transcription regulation, vascular smooth muscle cell apoptosis, lipid metabolism, cellular heterogeneity, foam cells, single-cell R. N. A. sequencing, calcific aortic valve disease, vascular smooth muscle cells, S. R. minus B. 1 protein, therapeutic targets, atherosclerosis, B. M. A. L. 1, low-density lipoprotein cholesterol, GPR146, aortic development, ChemR23, thoracic aortic aneurysm, aortic homeostasis, aortic dissection, smooth muscle cells, T. B. X. 18, phenotypic switching, high-density lipoprotein cholesterol.
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Concise summaries of cardiovascular research for professionals.
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