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Interferon regulatory factor-5-dependent CD11c+ macrophages contribute to the formation of rupture-prone atherosclerotic plaques.

Andreas EdsfeldtMaarten SwartPratibha SinghLea DibJiangming SunJennifer E ColeInhye ParkDania Al-SharifyAna PerssonMihaela NitulescuPatricia Das Neves BorgesChristina KassiteridiMichael E GoddardRegent LeePetr VolkovMarju Orho-MelanderLars MaegdefesselJan NillsonIrina UdalovaIsabel GoncalvesClaudia Monaco
Published in: European heart journal (2022)
Using complementary evidence from data from human carotid endarterectomies and a murine model of inducible rupture of carotid artery plaque in IRF5-deficient mice, we demonstrate a mechanistic link between the pro-inflammatory transcription factor IRF5, macrophage phenotype, plaque inflammation, and its vulnerability to rupture.
Keyphrases
  • transcription factor
  • dendritic cells
  • coronary artery disease
  • endothelial cells
  • oxidative stress
  • climate change
  • adipose tissue
  • big data
  • immune response
  • genome wide identification