Clint L. Miller

The paper identifies 16 genetic loci interacting with sleep duration to influence glycemic traits in over 480,000 individuals, revealing distinct biological mechanisms for short and long sleep.

This study identifies METTL7A as a mechanosensitive methyltransferase that regulates internal m7G methylation in endothelial cells, protecting against atherosclerosis through stabilization of anti-inflammatory transcripts.

This study integrates CAD GWAS with transcriptomic data to identify genes and networks associated with CAD and subclinical atherosclerosis.

Smooth muscle foam cells in early-to-intermediate human coronary plaques map to fibromyocytes, express CFH and SERPINE1 unlike macrophage foam cells, and show matrix, coagulation and angiogenesis programs.

This study identifies desert hedgehog (DHH) as a resilience factor that prevents atherosclerosis by inhibiting PAI-1 signaling and endothelial mesenchymal transition.

This study uses single-cell multi-omics to show that diabetic mice show persistent aortic smooth muscle cell dysfunction and phenotypic changes despite glycemic control, with partial reversal by dapagliflozin.

This study shows PRDM16 maintains SMC identity and regulates atherosclerotic plaque composition by inhibiting synthetic gene programs during SMC fate switching.

The paper links ADAR1-mediated RNA editing in smooth muscle cells to regulation of MDA5 activation, showing its role in atherosclerosis progression and vascular calcification.

This study identifies FNDC1 as a key regulator of vascular calcification through the FNDC1-NAMPT-NAD axis, showing its role in both microvascular and macrovascular diseases and its potential as a therapeutic target.

The paper investigates how genetic regulation of tissue expression influences chronic wound microbiome composition through a microbiome-transcriptome-wide association study.

This study identifies 22 novel gene-sleep duration interaction loci for blood pressure traits across 811,405 individuals, highlighting distinct genetic influences of short and long sleep on cardiovascular health.

This study shows that endothelial MICU1 prevents vascular inflammation and atherosclerosis by maintaining mitochondrial calcium homeostasis and reducing mitochondrial reactive oxygen species.

This study shows that the 9p21.3 CAD risk locus drives vascular smooth muscle cells to an osteochondrogenic state through ANRIL expression, leading to arterial calcification.

This study shows that interferon-induced H3K9me3 and ATRX restrict HSV-1 reactivation by maintaining epigenetic memory during neuronal latency.

This paper links CAD GWAS variants to causal genes in SMCs using single-cell chromatin accessibility and Hi-C data, creating a scV2E2G map for disease mechanism discovery.

This study identifies BST2 as a driver of vascular smooth muscle cell plasticity and macrophage-like phenotype switching in tumors, with implications for immunosuppression and therapy.

This study shows that a polygenic risk score for coronary artery disease is associated with more severe atherosclerosis features in autopsy samples of sudden death cases.

This study performs a meta-analysis of scRNA-seq datasets to map human atherosclerosis cell diversity and identifies disease-relevant vascular cell states and markers.

This paper identifies INKILN, a human-specific lncRNA that promotes vascular smooth muscle inflammation by stabilizing MKL1 and interacting with USP10.

This study uses GWAS and Mendelian randomization to show that lower sclerostin levels increase risk of hypertension, type 2 diabetes, myocardial infarction, and atherogenic lipid profiles.

This study identifies FHL5 as a causal gene for vascular disease risk through eQTL colocalization and functional analyses, showing its role in vascular remodeling and calcification.

The paper uses single-cell ATAC-seq to analyze coronary artery cells from CAD patients, identifying regulatory mechanisms and risk variants associated with disease.

The paper identifies eQTLs and sQTLs in human aortic SMCs that colocalize with CAD GWAS loci, highlighting splicing regulation as a mechanism for CAD risk.

The paper introduces DeepVHPPI, a deep learning framework for predicting virus-host protein interactions for novel virus sequences, showing significant improvements over existing methods for SARS-CoV-2, H1N1, and Ebola.

The paper shows that dysfunctional vascular smooth muscle cells contribute to neuroinflammation and Tau hyperphosphorylation in Alzheimer's disease through phenotypic transitions and loss of contractile markers.

The paper applies an enhanced scRNA-seq workflow to human coronary artery data, revealing SMC transitions and drug targets through ligand-receptor analysis and an interactive web tool.

The paper identifies noncoding RNAs as key mediators linking coronary artery disease GWAS variants to causal genes.

The paper identifies five genes modulating coronary artery disease risk through smooth muscle cells by integrating eQTL and GWAS data with transcriptomic and epigenomic analyses.

BART predicts functional transcription factors regulating a gene set or associated with a genomic profile using existing ChIP-seq data.