NF-κB activation in cardiac fibroblasts results in the recruitment of inflammatory Ly6C ^hi monocytes in pressure-overloaded hearts

Abstract

monocyte recruitment and preserved cardiac function in mice subjected to pressure overload. Pseudotime analysis indicated two single-branch trajectories from quiescent fibroblasts into inflammatory fibroblasts and myofibroblasts. Our results provide insight into the mechanisms underlying cardiac inflammation and fibroblast-mediated inflammatory responses that could be therapeutically targeted to treat heart failure.