Research Highlights

Welcome to The Gupte Lab, where our mission is to advance the field of pharmacology through innovative research and collaborative efforts. Dive into our latest studies and explore the remarkable contributions of our dedicated team.

Loss-of-function G6PD variant moderated high-fat diet-induced obesity, adipocyte hypertrophy, and fatty liver in male rats

Authors: Shun Matsumura, Christina Signoretti, Samuel Fatehi, Bat Ider Tumenbayar, Catherine D'Addario, Erik Nimmer, Colin Thomas, Trisha Viswanathan, Alexandra Wolf, Victor Garcia, Petra Rocic, Yongho Bae, Sm Shafiqul Alam, Sachin A Gupte Obesity contributes to liver and cardiovascular diseases, but the underlying multi‑organ mechanisms remain unclear. This study shows that glucose‑6‑phosphate dehydrogenase (G6PD), a key enzyme in the pentose phosphate pathway, drives obesit

G6pdN126D Variant Increases the Risk of Developing VEGFR (Vascular Endothelial Growth Factor Receptor) Blocker-Induced Pulmonary Vascular Disease

Authors: Christina Signoretti, Shun Matsumura, Samuel Fatehi, Melinee D'Silva, Rajamma Mathew, Francesca Cendali, Angelo D'Alessandro, S M Shafiqul Alam, Victor Garcia, Joseph M Miano, Sachin A Gupte This study examined the role of an X-linked G6PD variant (N126D), prevalent in individuals of African ancestry, in vascular endothelial growth factor receptor blocker–induced pulmonary hypertension. Using CRISPR-engineered rats, we found that the G6PDN126D variant exacerbated pul

Bleomycin-induced lung fibrosis and dysfunction is exacerbated by G6PD deficiency

Authors: Christina Signoretti, Samuel Fatehi, Rhonda Drewes, Francesca Cendali, Monika Dzieciatkowska, Angelo D'Alessandro, Yongho Bae, Sachin A Gupte Summary: Pulmonary fibrosis is driven in part by oxidative stress and altered metabolism, yet the role of glucose metabolism in extracellular matrix (ECM) synthesis remains unclear. Using a bleomycin-induced rat model, we found that a loss-of-function G6PD variant (G6PDS188F) markedly exacerbates lung fibrosis compared with wil