PhysiologybioRxivPreprint
Mitochondrial Pyruvate Carrier Inhibition Attenuates Hepatic Stellate Cell Activation and Liver Injury in a Mouse Model of Metabolic Dysfunction-associated Steatotic Liver Disease
DOI 10.1101/2023.02.13.528384
Author
T. M. Shew
Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.
Biology Disciplines
Click to filter author papersSignature Assays, Organisms & Methods
Click to filter · or open tagActivity by Year
2020-2023 · peak 2/yrCo-Author Collaboration Network
10 top collaborators · 26 mutual co-author linksFocal author (center)Selected co-authorORCID co-authorUnlinked name
Curved chords = mutual co-authorship5 papers
Recent·Most cited
- PhysiologybioRxivPreprint
Adipocyte lipin 1 is positively associated with metabolic health in humans and regulates systemic metabolism in mice.
A. LaPoint, J. M. Singer, D. Ferguson…·A. J. Lutkewitte
The paper shows that lower adipose lipin 1 in humans correlates with metabolic issues, and mice lacking adipocyte lipin 1 develop metabolic disorders.
- Cell BiologybioRxivPreprint
Monoacylglycerol disrupts Golgi structure and perilipin 2 association with lipid droplets
L.-A. L. S. Harris, J. R. Skinner, T. M. Shew…·N. Wolins
This study shows that monoacylglycerols disrupt Golgi structure and perilipin 2 association with lipid droplets in enterocytes and fibroblasts.
DOI 10.1101/2021.07.09.451829 - PhysiologybioRxiv
Antisense oligonucleotides against monoacylglycerol acyltransferase 1 (Mogat1) improve glucose metabolism independently of Mogat1
A. J. Lutkewitte, J. M. Singer, T. M. Shew…·B. N. Finck
This study shows that Mogat1 ASOs improve glucose metabolism in mice independently of Mogat1 knockdown or IFNAR-1 activation.
DOI 10.1016/j.molmet.2021.101204 - PhysiologybioRxiv
Ketogenic Diet Prevents Heart Failure from Defective Mitochondrial Pyruvate Metabolism
K. S. McCommis, A. Kovacs, C. J. Weinheimer…·B. N. Finck
This study shows that a ketogenic diet prevents heart failure in mice with defective mitochondrial pyruvate metabolism by reversing cardiac remodeling and dysfunction.
DOI 10.1038/s42255-020-00296-1