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Bridget Simonson

As seen in: Science Magazine, BioRxiv, Cell Reports
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Articles by Bridget Simonson

Single cell transcriptomic analyses of human heart failure with preserved ejection fraction

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By Virginia Shalkey Hahn, Mark Chaffin, Bridget Simonson, Sydney Jenkin
| BioRxiv
Abstract Background: Heart failure with preserved ejection fraction (HFpEF) is a poorly understood, multi-system disease with high morbidity and mortality. To improve our understanding of its underlying biology, we used single-nucleus RNA sequencing (snRNA-seq) to characterize cell-specific gene expression patterns in human HFpEF myocardium.
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Single-nucleus RNA sequencing in ischemic cardiomyopathy reveals common transcriptional profile underlying end-stage heart failure

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By Bridget Simonson, Mark Chaffin, Matthew Hill, Ondine Atwa
| Cell Reports Verified
1 Global epidemiology of ischemic heart disease: results from the global burden of disease study. ICM is most commonly caused by atherosclerotic coronary artery disease inhibiting blood flow to the heart. This leads to decreased oxygen in the myocardium causing cardiomyocyte death and cardiac remodeling via formation of a fibrotic scar. Over time the lack of oxygen and formation of the scar leads to a loss of contractile function, cardiac hypertrophy, dilation, and heart failure.
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Aortic Cellular Diversity and Quantitative Genome-Wide Association Study Trait Prioritization Through Single-Nuclear RNA Sequencing of the Aneurysmal Human Aorta

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By Elizabeth Chou, Mark Chaffin, Bridget Simonson, James P Pirruccello
| AHA/ASA Journals
Originally publishedhttps://doi.org/10.1161/ATVBAHA.122.317953Arteriosclerosis, Thrombosis, and Vascular Biology. 2022;42:1355–1374 Abstract Background: Mural cells in ascending aortic aneurysms undergo phenotypic changes that promote extracellular matrix destruction and structural weakening. To explore this biology, we analyzed the transcriptional features of thoracic aortic tissue.
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DDiT4L promotes autophagy and inhibits pathological cardiac hypertrophy in response to stress

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By Vinita Subramanya, Bridget Simonson, Mun Chun Chan, Aifeng Zhang
| Science Magazine Verified
An increase in workload causes the heart to enlarge. When this occurs in response to good stress (exercise or pregnancy), this is beneficial or adaptive hypertrophy; when this occurs in response to bad stress (high blood pressure or poor heart function), this process is pathological and contributes to heart failure. The kinase mTOR functions in two complexes: mTORC1, which promotes cell growth, and mTORC2, which promotes cytoskeletal rearrangements. Simonson et al.
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