NF-κB activation in cardiac fibroblasts results in the recruitment of inflammatory Ly6Chi monocytes in pressure-overloaded hearts in mice.
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.
Abe et al. (Tue,) conducted a other in Heart failure / Pressure overload. NF-κB activation in cardiac fibroblasts was evaluated on Monocyte recruitment and cardiac function. NF-κB activation in cardiac fibroblasts results in the recruitment of inflammatory Ly6Chi monocytes in pressure-overloaded hearts in mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: