NF-κB activation in cardiac fibroblasts results in the recruitment of inflammatory Ly6C <sup>hi</sup> monocytes in pressure-overloaded hearts
Hajime Abe, Yohei Tanada, Shigemiki Omiya, Mihai‐Nicolae Podaru, Tomokazu Murakawa, Jumpei Ito, Ajay M. Shah, Simon J. Conway, Masahiro Ono, Kinya Otsu
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.
Topics & Concepts
ChemokinePressure overloadInflammationMonocyteFibroblastCCL2Activator (genetics)Transcription factorHeart failureCell biologyNFKB1BiologyImmunologyCancer researchMedicineInternal medicineGeneReceptorCell cultureCardiac hypertrophyBiochemistryGeneticsCardiac Fibrosis and RemodelingSignaling Pathways in DiseaseNF-κB Signaling Pathways