Maxwell La Forest
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Maxwell La Forest has a total of 26 co-authors. Here are the top co-authors by number of shared publications:
- Edward A. Fisher
Division of Cardiology, Department of Medicine, New York University Grossman School of Medicine, New York, USA
2 shared publications Adam A. Ghotbi
Biomedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, USA
1 shared publication- Ben Readhead
ASU‐Banner Neurodegenerative Disease Research Center Arizona State University Tempe Arizona USA
1 shared publication - Chiara Giannarelli
Department of Medicine, Division of Cardiology, NYU Cardiovascular Research Center, NYU Grossman School of Medicine, NYU Langone Health, New York, USA
1 shared publication - Christopher A. Hill
Department of Medicine, Division of Cardiology, Icahn School of Medicine at Mount Sinai, New York, USA
1 shared publication Christopher Faries
Biomedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, USA
1 shared publication
Latest Publications
- Open Access
- 2 September 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Gene regulatory network analysis identifies auranofin as an anti-atherosclerotic drug
Gene-regulatory networks (GRNs) offer a mechanistic framework for dissecting the complex molecular and genetic architecture of coronary artery disease and for identifying new therapeutic opportunities. Here, we present a GRN-driven drug-repurposing strategy that integrates transcriptional signatures induced by silencing key drivers of the human arterial wall foam cell regulator GRN 42 with drug-induced gene expression profiles from the NIH LINCS program. In vitro screening of top candidate compounds validates the computational predictions, identifying candidate foam cell modulators and showing that auranofin, an FDA-approved gold salt used to treat rheumatoid arthritis, effectively reduces foam cell formation. In vivo, auranofin attenuates atherosclerosis and inflammation in both male mice and rabbits. Clinically, auranofin was associated with reduced cardiovascular risk in a retrospective cohort of patients with rheumatoid arthritis. Together, these findings show that a GRN-based drug-repurposing framework, coupled with preclinical and clinical validation, can uncover new therapeutic applications for existing drugs, including auranofin, in coronary artery disease.
- 2 September 2026
- Published by Springer Nature in Nature Communications
- Vol. 17 (1)
Open AccessGene regulatory network analysis identifies auranofin as an anti-atherosclerotic drug
Gene-regulatory networks (GRNs) offer a mechanistic framework for dissecting the complex molecular and genetic architecture of coronary artery disease and for identifying new therapeutic opportunities. Here, we present a GRN-driven drug-repurposing strategy that integrates transcriptional signatures induced by silencing key drivers of the human arterial wall foam cell regulator GRN 42 with drug-induced gene expression profiles from the NIH LINCS program. In vitro screening of top candidate compounds validates the computational predictions, identifying candidate foam cell modulators and showing that auranofin, an FDA-approved gold salt used to treat rheumatoid arthritis, effectively reduces foam cell formation. In vivo, auranofin attenuates atherosclerosis and inflammation in both male mice and rabbits. Clinically, auranofin was associated with reduced cardiovascular risk in a retrospective cohort of patients with rheumatoid arthritis. Together, these findings show that a GRN-based drug-repurposing framework, coupled with preclinical and clinical validation, can uncover new therapeutic applications for existing drugs, including auranofin, in coronary artery disease.