Author

Qi Cai

Primary ORCID profile (0000-0002-4820-805X · 5 papers)Unclaimed ORCID profile · follow to get notified of new preprints

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Same name, identified by ORCID

Qi CaiiD5 papers · The University of Texas at Dallas

Biology Disciplines

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Cell Biology· 1 Pathology· 1

Signature Assays, Organisms & Methods

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Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Approach:deep learning· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Adam Burgess· 1 shared Akhil AmbekariD· 1 shared Alison Bunio AlveariD· 1 shared Andreas BueckleiD· 1 shared Andrew J. BarkmeieriD· 1 shared Andrew S. BombackiD· 1 shared Angela R. SaboiD· 1 shared Ashley Berglund· 1 shared

Activity by Year

2016-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperCell Biology

Adam Burgess

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Author profile →

2 papers

Recent·Most cited

A MEF2C transcription factor network regulates proliferation of glomerular endothelial cells in diabetic kidney disease

Ricardo Melo Ferreira, Debora L. Gisch, Carrie L. Phillips, Ying‐Hua Cheng, Nicholas Lucarelli, Soumya Yennapureddy, Maansi Asthana, Blue B. Lake, William S. Bowen, Fang Fang, Mahla Asghari, Angela R. Sabo, Daria Barwinska, Michael J. Ferkowicz, Robert D. Toto, , Tashas Cameron-Wheeler

This study identifies a MEF2C transcription factor network that regulates endothelial cell proliferation in diabetic kidney disease and shows that SGLT2i treatment can reverse its dysregulation.

Kidney International · Apr 27, 2026Peer-reviewedCell Biology

GPR4 Deficiency Alleviates Intestinal Inflammation in a Mouse Model of Inflammatory Bowel Disease

Edward J Sanderlin, Nancy R Leffler, Kvin Lertpiriyapong, Qi Cai, Heng Hong, Vasudevan Bakthavatchalu, James G Fox, Joani Zary Oswald, Calvin R Justus, Elizabeth A Krewson, Dorcas O'Rourke, Li V Yang

This study shows that GPR4 deficiency reduces intestinal inflammation in a DSS-induced colitis mouse model by decreasing inflammation, leukocyte infiltration, and ILF formation.

bioRxiv · Jun 14, 2016Pathology