Fernando Neto/van Berlo Lab Identify Key Immune Driver in Heart Failure Progression
A new study from the van Berlo lab, published in JACC: Basic to Translational Science, has identified a pivotal mechanism linking immune signaling to heart failure. Lead author and American Heart Association-supported postdoctoral fellow Fernando Neto, PhD demonstrated that the macrophage-derived chemokine CXCL10 serves as a central regulator of pathological cardiac remodeling. Using pressure-overload models, the research team found that CXCL10 is significantly upregulated in cardiac macrophages. Their findings reveal that this chemokine doesn't just signal the presence of stress but actively drives hypertrophy, fibrosis, and progressive systolic dysfunction. Specifically, the study expands our understanding of "neuroinflammation" by highlighting how CXCL10 orchestrates critical communication between macrophages and T cells.
By showing that the genetic deletion of CXCL10 blunts these damaging effects, the work establishes a new potential therapeutic target. This discovery offers a significant step forward in understanding the immune-mediated pathways that govern heart failure, suggesting that modulating this specific macrophage-T cell axis could mitigate disease progression.
