Author

Si Young An

Northwestern UniversityORCID 0000-0002-9409-1307Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Edward Benjamin ThorpiD· 2 shared Gabriella S. Borkowski· 2 shared Navdeep S. ChandeliD· 2 shared Pinelopi P. KapitsinouiD· 2 shared Rajni SharmaiD· 2 shared Ratnakar TiwariiD· 2 shared Susan E. QuagginiD· 2 shared Yalu Zhou· 2 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersMolecular Biology

Edward Benjamin ThorpORCID

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2 papers

Recent·Most cited

Endothelial Prolyl Hydroxylase 3 Mitigates Maladaptive Inflammation to Promote Post-Ischemic Kidney Repair

Rajni Sharma, Ratnakar Tiwari, Yalu Zhou, James O'Sullivan, Hiroshi Maekawa, Gabriella S. Borkowski, Haris Bukaric, Si Young An, Edward Benjamin Thorp, Navdeep S. Chandel, Susan E. Quaggin, Pinelopi P. Kapitsinou

This study identifies endothelial PHD3 as a regulator of kidney repair after ischemia, showing its role in suppressing inflammation and fibrosis through HIF-dependent mechanisms.

Kidney International · Feb 14, 2026Peer-reviewedMolecular Biology

Post-ischemic inactivation of HIF prolyl hydroxylases in endothelium promotes maladaptive kidney repair by inducing glycolysis

Ratnakar Tiwari, Rajni Sharma, Ganeshkumar Rajendran, Gabriella S. Borkowski, Si Young An, Michael P. Schonfeld, James O’Sullivan, Matthew John Schipma, Yalu Zhou, Guillaume Courbon, Benjamin R. Thomson, Valentin David, Susan E. Quaggin, Edward Benjamin Thorp, Navdeep S. Chandel, Pinelopi P. Kapitsinou

This study shows that inactivating PHD enzymes in endothelial cells after ischemic kidney injury promotes maladaptive repair through glycolysis and MCT4, which can be reversed by MCT4 inhibitors.

Journal of Clinical Investigation · Dec 2, 2024Peer-reviewedMolecular Biology