iNOS aggravates pressure overload-induced cardiac dysfunction via activation of the cytosolic-mtDNA-mediated cGAS-STING pathway
Yongzheng Guo, Yuehua You, Fei‐Fei Shang, Xiaowen Wang, Bi Huang, Boying Zhao, Dingyi Lv, Shenglan Yang, Ming Xie, Lingwen Kong, Dingyuan Du, Suxin Luo, Xin Tian, Yong Xia
Abstract
Our findings demonstrate that mtDNA is released into the cytosol and triggers sterile inflammation through the cGAS-STING pathway leading to cardiac dysfunction after pressure overload. iNOS controls mtDNA release and subsequent cGAS activation in pressure-stressed hearts.
Topics & Concepts
InflammationPressure overloadMitochondrionProinflammatory cytokineCell biologyStingCytosolNitric oxide synthasePathogenesisBiologyMedicineInternal medicineImmunologyEndocrinologyHeart failureNitric oxideBiochemistryEnzymeAerospace engineeringEngineeringCardiac hypertrophyinterferon and immune responsesInflammasome and immune disordersImmune cells in cancer