TWEAK/Fn14 signaling drives oxidative cardiac injury in systemic lupus erythematosus: Evidence from patient biomarker studies, lupus mouse models, and cardiomyocyte assays. | Synapse
February 28, 2026
TWEAK/Fn14 signaling drives oxidative cardiac injury in systemic lupus erythematosus: Evidence from patient biomarker studies, lupus mouse models, and cardiomyocyte assays.
Key Points
To investigate the role of TWEAK/Fn14 signaling in oxidative cardiac injury associated with systemic lupus erythematosus.
Analysis of patient biomarkers related to TWEAK/Fn14 signaling
Use of lupus mouse models to study cardiac injury mechanisms
In vitro cardiomyocyte assays to assess oxidative stress effects
Identified increased oxidative stress markers in cardiac tissues of lupus patients
Demonstrated that TWEAK/Fn14 signaling contributes significantly to cardiomyocyte injury
Proposed TWEAK/Fn14 as a promising biomarker and target for therapeutic interventions.
Abstract
TWEAK/Fn14 signaling drives oxidative stress- mediated cardiomyocyte injury in SLE and represents a promising biomarker and therapeutic target for lupus-associated cardiac damage.