Gökhan M. Mutlu

The paper investigates sex-specific molecular responses to early-life toxicant exposures in mice across multiple life stages using transcriptomic and epigenomic data.

The paper uses transfer learning to predict drug-target interactions for mitochondrial one-carbon metabolism enzymes with limited data, identifying potential repurposable drugs.

This study shows that mitochondrial one-carbon metabolism is essential for TGF-β-induced glycine synthesis and collagen production in lung fibroblasts, suggesting MTHFD2 inhibitors could treat IPF.

The paper characterizes persistent epigenomic and transcriptomic changes in mice exposed to environmental toxicants across life stages, revealing widespread gene expression and chromatin alterations.

This study investigates the role of arginine and its metabolism in TGF-β-induced activation of lung fibroblasts, finding that arginine depletion inhibits mTORC1 activation and collagen production.

The paper shows early-life toxicant exposure reprograms epigenomic aging, altering gene expression in liver cells and disease risk in adulthood.

The paper shows HIF-1α regulates glycolytic shifts and mitochondrial function differently in bone marrow-derived macrophages compared to tissue-resident alveolar macrophages.

This paper develops a modular nanoparticle platform for targeted mRNA delivery to inflamed endothelial cells, showing efficacy in treating ARDS and atherosclerosis by restoring disease-related gene pathways.

This study investigates how ATF4 and mTOR regulate metabolic reprogramming in TGF-β-treated lung fibroblasts, identifying their roles in amino acid homeostasis and glycolytic pathways.

This study shows that Gα12 and Gα13 proteins are essential for TGF-β-induced myofibroblast differentiation by regulating Smad phosphorylation and receptor expression.

This study shows that Decitabine can reactivate FoxM1-dependent vascular repair in aged mice, improving survival after sepsis and suggesting potential treatment for elderly ARDS and COVID-19 patients.

Single-cell RNA-seq of lung tissue from transplant donors, fibrosis patients, and a living patient identifies cell type-specific disease-associated molecular pathways in pulmonary fibrosis.