Author

Sandeep Krishna Agarwal

Baylor College of MedicineORCID 0000-0002-0053-2803Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Approach:deep learning· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Alan WaichiD· 2 shared Cristian CoarfaiD· 2 shared Iván O. RosasiD· 2 shared Juan D. ZuluagaiD· 2 shared Lindsay J. CeladaiD· 2 shared Neil J. McKennaiD· 2 shared Scott A. OchsneriD· 2 shared A. Brent CarteriD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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2 shared papersMolecular Biology

Alan WaichORCID

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2 papers

Recent·Most cited

Mechanosignaling Promotes Macrophage Apoptosis Resistance in Pulmonary Fibrosis via Metabolic Reprogramming

Chao He, Cristian Coarfa, Neftali Garcia, O Lebimoyo, Haiwei Gu, Elisa Ruiz-Echartea, Xiaoli Ji, Alan Waich, Juan D. Zuluaga, Lindsay J. Celada, Scott A. Ochsner, Neil J. McKenna, Jennifer L. Larson‐Casey, Sandeep Krishna Agarwal, Farrah Kheradmand, , Iván O. Rosas

This study shows that mechanical stiffness in fibrotic lungs promotes macrophage apoptosis resistance through metabolic reprogramming, contributing to fibrosis progression.

bioRxiv · Sep 28, 2026 · PreprintMolecular Biology

Single cell transcriptomics in a treatment-segregated cohort exposes a STAT3-regulated therapeutic gap in idiopathic pulmonary fibrosis

Neil J. McKenna, Scott A. Ochsner, Alan Waich, Juan Cala-García, Maria E. Ruiz Echartrea, Sandra L. Grimm, Fernando Poli, Rafael Cardenas Castillo, Juan D. Zuluaga, Sergio Poli, Taylor Sterling Adams, Ricardo Pineda, B.J. Moss, Tianshi David Wu, Charles G. Minard, , Iván O. Rosas

The paper uses single-cell transcriptomics to analyze an IPF cohort, revealing a transcriptional deficit refractory to current treatments and identifying STAT3 as a key regulator in the therapeutic gap.

bioRxiv · Jun 16, 2025 · PreprintCell Biology