PubRank

TWEAK/Fn14 interaction promotes oxidative stress through NADPH oxidase activation in macrophages.

PubWeight™: 0.78‹?›

🔗 View Article (PMID 26224570)

Published in Cardiovasc Res on July 29, 2015

Authors

Julio Madrigal-Matute1, Valvanera Fernandez-Laso2, Cristina Sastre2, Patricia Llamas-Granda2, Jesús Egido2, José Luis Martin-Ventura2, Guillermo Zalba3, Luis Miguel Blanco-Colio4

Author Affiliations

1: Vascular Research Lab, IIS-Fundación Jiménez Díaz, Autonoma University, Av. Reyes Católicos 2, 28040 Madrid, Spain Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
2: Vascular Research Lab, IIS-Fundación Jiménez Díaz, Autonoma University, Av. Reyes Católicos 2, 28040 Madrid, Spain.
3: Division of Cardiovascular Sciences, CIMA University of Navarra, Pamplona, Spain Department of Biochemistry and Genetics, University of Navarra, Pamplona, Spain.
4: Vascular Research Lab, IIS-Fundación Jiménez Díaz, Autonoma University, Av. Reyes Católicos 2, 28040 Madrid, Spain lblanco@fjd.es.

Articles citing this ↘

TWEAK blockade decreases atherosclerotic lesion size and progression through suppression of STAT1 signaling in diabetic mice. Sci Rep (2017) 0.75

TWEAK/Fn14 Activation Participates in Skin Inflammation. Mediators Inflamm (2017) 0.75

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors. Exp Ther Med (2017) 0.75