Author

Zu‐Xi Yu

National Institutes of HealthORCID 0000-0002-1341-4486Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

Zu‐Xi Yu1 paper · National Institutes of Health

Biology Disciplines

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Developmental Biology· 1 Molecular Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 3 Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Research Focus:gene regulatory network inference· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:clustering· 1

Frequent Co-Authors

Danielle SpringeriD· 2 shared Alan Thomas RemaleyiD· 1 shared Apratim MitraiD· 1 shared Avi Z. RosenbergiD· 1 shared Beenish RahatiD· 1 shared Beth A. KozeliD· 1 shared Bibiana BielekovaiD· 1 shared Charles NatansoniD· 1 shared

Activity by Year

2021-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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2 shared papersMolecular Biology

Danielle SpringerORCID

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3 papers

Recent·Most cited

PhysiologybioRxivPreprintJul 7, 2025

Myocyte Damage and Mass Loss Drives Increasing Water Content, Compliance, and Survival in Septic Cardiomyopathy

Verity J. Ford, Steven B. Solomon, Junfeng Sun…·Charles Natanson

This paper investigates how myocyte damage and mass loss in septic cardiomyopathy affect left ventricular compliance, water content, and survival outcomes.

DOI 10.1101/2025.07.07.663608

imagingexperimental assay

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Molecular BiologyClinical SciencePeer-reviewedJun 1, 2025

Apolipoprotein-L1 G1 variant contributes to hydrocephalus but not to atherosclerosis in apolipoprotein-E knock-out mice

Teruhiko Yoshida, Zhi-Hong Yang, Shinji Ashida…·Jeffrey B. Kopp

The paper investigates the role of APOL1 variants in cardiovascular and neurological diseases using mice, finding APOL1-G1 contributes to hydrocephalus but not atherosclerosis.

DOI 10.1042/cs20255324

mousebulk RNA-seq

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Developmental BiologyeLifePeer-reviewedAug 17, 2021

Cardiac pathologies in mouse loss of imprinting models are due to misexpression of H19 long noncoding RNA

Ki-Sun Park, Beenish Rahat, Hyung Chul Lee…·Karl E. Pfeifer

The paper shows that maternal loss of imprinting at the H19/IGF2 locus causes cardiac pathologies in mice, with Igf2 driving transient hypertrophy and H19 causing progressive fibrosis and reduced ventricular function.

14 citations

mouseexperimental assay

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