Myeloid Cell Expansion Propels Right Ventricular Dysfunction in HFpEF Through Sterile Inflammation.
Myeloid cell expansion directly contributes to right ventricular dysfunction in HFpEF, with a 40% increase in leukocyte infiltration observed in affected mice and humans.
- Why it matters: Understanding the immune mechanisms behind RVD in HFpEF is crucial because current models lack clarity, hindering targeted therapies for this common heart failure subtype.
- What they did: Researchers developed a murine HFpEF model with RVD, analyzed human HFpEF tissue, and used colony-stimulating factor 1 receptor inhibitors to deplete myeloid cells, assessing their role in RV remodeling.
- The result: Depleting myeloid cells reduced RV systolic pressure and dysfunction, revealing that dysregulated myeloid cell activity drives RVD, which could inform new anti-inflammatory treatments for HFpEF.