Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages.
By M. Kratz, Brittney R. Coats, K. Hisert, D. Hagman, Vesco Mutskov, E. Peris, K. Schoenfelt, J. Kuzma, Ilona Larson, P. Billing and 6 more. Cell Metabolism, 2014
738 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/c7e4e8ed063ce4528f752273023c89f14b2d726f
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
In Immunology
- F. Munari
- R. Sánchez-Rodríguez
- Tommaso Scolaro
- M. Colonna
- A. Viola
- Florent Ginhoux
- Mitchell A. Lazar
- Eran Elinav
In Molecular Biology
- Eran Elinav
- Hadas Keren-Shaul
- Eyal David
- M. Colonna
- Ido Amit
- Mitchell A. Lazar
- A. Chait
- Diego Jaitin
Citations in the corpus
- The Metabolic Signature of Macrophage Responses (2019, background): “Fatty acids and TNF-α have been shown to induce M1 polarization in obesity (165) but also glucose, insulin, and obesity-induced hypoxia trigger macrophages toward a pro-inflammatory phenotype (169).”
- Lipid-associated macrophages control metabolic homeostasis in a Trem2-dependent manner (2019, background): “, 2013), and with the notion of “metabolically-activated” adipose tissue macrophages (Hill et al., 2018; Kratz et al., 2014; Xu et al., 2013).”
- Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease (2020, background): “Such markers of metabolic activation were expressed by pro-inflammatory macrophages in adipose tissue from obese humans and mice and correlated with the extent of adiposity (225).”