Author

Jonghae Lee

The University of Texas MD Anderson Cancer CenterORCID 0000-0002-1182-9653Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Organism:human· 2 Research Focus:cell signaling & trafficking· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Assay:metabolomics· 1 Organism:mouse· 1

Frequent Co-Authors

Anita M DeswaliD· 2 shared Efstratios KoutroumpakisiD· 2 shared Gilbert F. MejiaiD· 2 shared Guangyu WangiD· 2 shared Jared K. BurksiD· 2 shared Joerg HerrmanniD· 2 shared Jun‐ichi AbeiD· 2 shared Keila Carolina Ostos MendozaiD· 2 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCell Biology

Anita M DeswalORCID

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2 papers

Recent·Most cited

Colchicine Directly Targets Aldehyde Dehydrogenase 2 (ALDH2) to Suppress Radiation-Induced Senescence and Atherosclerosis

Jun‐ichi Abe, Venkata Subrahman K Samanthapudi, Weiqing Chen, Jonghae Lee, Ngoc Tuyet Tra, Gilbert F. Mejia, Oanh N. Hoang, Luis Antonio Rivera, Kun Yuan Chu, Masaki Osawa, Jung Hyun Kim, Shengyu Li, Kyung Ae Ko, Anilkumar K. Reddy, Silvia Fernanda López Moreno, , Sivareddy Kotla

This study identifies ALDH2 as a direct target of colchicine, showing it suppresses radiation-induced senescence and atherosclerosis by modulating mitochondrial redox and macrophage function.

bioRxiv · May 30, 2026 · PreprintCell Biology

Downregulation of LATS1/2 Drives Endothelial Senescence-Associated Stemness (SAS) and Atherothrombotic Lesion Formation

Sivareddy Kotla, Jonghae Lee, Kyung Ae Ko, Weiqing Chen, Venkata Subrahman K Samanthapudi, Oanh N. Hoang, Gilbert F. Mejia, Shengyu Li, Keri Schadler, Luis Antonio Rivera, Masaki Imanishi, Kay Carlene Tavares Samperio, Jung Hyun Kim, Keila Carolina Ostos Mendoza, Karla N. Mariscal-Reyes, , Jun‐ichi Abe

This study shows that loss of LATS1/2 in endothelial cells promotes a senescence-associated stemness (SAS) state, leading to atherothrombotic plaque formation through metabolic and mitochondrial dysregulation.

bioRxiv · Jun 19, 2025 · PreprintMolecular Biology