Article in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
14 authors.
Lucie Y ZhuDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).ORCID 0000-0002-1048-5377
Chenyi XueDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).ORCID 0000-0002-8829-7659
Alexander C BashoreDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).ORCID 0000-0002-1380-9242
Jian CuiDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).
Sicong YaoDepartment of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA (S.Y., M.L.).
Nadja SachsDepartment of Vascular and Endovascular Surgery, TUM University Hospital Klinikum, Technical University Munich, Germany (N.S.).ORCID 0000-0001-8031-017X
Justus L WettichInstitute of Molecular Vascular Medicine, TUM University Hospital Klinikum, Technical University Munich, Germany (J.L.W., L.M.).ORCID 0009-0006-2008-1049
Johana CoronelDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).ORCID 0000-0002-9257-0849
Enrique J GarciaDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).ORCID 0000-0002-4779-5766
Shareef KhalidDepartment of Medicine, Columbia University Irving Medical Center, New York, NY (S.K., D.S., M.P.R.).
Danish SaleheenDepartment of Medicine, Columbia University Irving Medical Center, New York, NY (S.K., D.S., M.P.R.).ORCID 0000-0001-6193-020X
Mingyao LiDepartment of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA (S.Y., M.L.).ORCID 0000-0003-2422-9494
Lars MaegdefesselInstitute of Molecular Vascular Medicine, TUM University Hospital Klinikum, Technical University Munich, Germany (J.L.W., L.M.).ORCID 0000-0001-5228-2634
Muredach P ReillyDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (L.Y.Z., C.X., A.C.B., J. Cui, J. Coronel, E.J.G., M.P.R.).ORCID 0000-0002-3035-9386
Funding
Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Clinical and Translational Science AwardUL1TR001873 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REILLY, MUREDACH P · 2016 to 2025
$99.0M
POSTDOCTORAL TRAINING IN ARTERIOSCLEROSIS RESEARCHT32HL007343 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HENRY N GINSBERG, Muredach P Reilly · 1985 to 2026
$12.7M
Smooth muscle cell-derived cell fates and cellular interactions in atherosclerotic plaque stability in disease progression and regression.R01HL166916 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Muredach P Reilly · 2023 to 2026
$2.8M
Identification of smooth muscle cell genes causal in atherosclerotic plaque stability and cardiovascular disease riskR01HL169766 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Muredach P Reilly, Danish Saleheen · 2023 to 2026
$2.6M
Integration of spatial transcriptomics, genetics, and histomorphology for causal inference in atherosclerotic cardiovascular diseaseR01HL171595 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Muredach P Reilly · 2024 to 2026
backgroundSmooth muscle cell (SMC)-derived cells form the bulk of cells in atherosclerotic lesions and modulate lesion stability and cardiovascular disease outcomes. Unfolded protein response (UPR) markers, thin fibrous caps, and inflammation correlate with human lesion instability and rupture. In mice, UPR drives macrophage and endothelial apoptosis and inflammation, but its impact on lesion stability through SMC modulation is debated. The UPR protein PERK (protein kinase RNA-like ER kinase) was recently shown to drive SMC modulation in vivo, suggesting that depletion of SMC Perk may regulate lesion stability.
methodsSMC Perk was deleted from SMC-lineage-traced adult Ldlr
resultsSMC Perk deletion in adult atherogenic mice did not affect weight gain or serum cholesterol levels. Lesions from Perk knockout mice resembled Perk WT counterparts with similar progression, lesion stability features, and cell populations. Scoring of UPR markers and differential expression analysis found little UPR activity in SMC and smooth muscle-derived cell populations. Perk was not required for in vitro SMC modulation in atherogenic conditions. No correlation was found between UPR markers and lesion stability or symptomatic clinical presentation in human carotid lesions, and UPR markers were expressed primarily in infiltrating leukocytes rather than in SMCs and stromal cells.
conclusionsSMC Perk UPR does not play a significant role in atherosclerotic SMC modulation, disease progression, or features of lesion stability in mice. Similarly, expression of markers of the Perk UPR pathway in humans does not correlate with human carotid lesion stability or clinical presentation.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
PERK Is Dispensable for Smooth Muscle Cell Phenotype Switching in Atherosclerosis. · full record | OpenQuestion