Lats2 deficiency protects the heart against myocardial infarction by reducing inflammation and inhibiting mitochondrial fission and STING/p65 signaling
Libao Liu, Shuai Huang, Yingzhen Du, Hao Zhou, Kai Zhang, Jinyuan He
Abstract
deficiency inhibited AMI/hypoxia-related mitochondrial fission and inactivated STING/p65 signaling by preventing hypoxia-induced release of mtDNA into the cytosol. Accordingly, pharmacological reactivation of STING signaling abolished the cardioprotective effects of Lats2 ablation. Those data suggest that AMI-induced Lats2 upregulation is associated with impaired cardiomyocyte viability and function resulting from enhanced mitochondrial fission, mtDNA release, and STING/p65 pathway activation.
Topics & Concepts
Mitochondrial fissionCardioprotectionMitochondrionSignal transductionBiologyDownregulation and upregulationCell biologyHypoxia (environmental)Cancer researchMedicinePharmacologyInternal medicineMyocardial infarctionChemistryBiochemistryGeneOrganic chemistryOxygeninterferon and immune responsesCancer-related molecular mechanisms researchNF-κB Signaling Pathways