Key result
NF-κB activation in cardiac fibroblasts results in the recruitment of inflammatory Ly6Chi monocytes in pressure-overloaded hearts in mice.
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Hypothesis-generating for inflammatory pathways in heart failure; does not support practice changes without human data.
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.
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Abe et al. (2021) studied 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.
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