TIGAR reduces smooth muscle cell autophagy to prevent pulmonary hypertension
Ryoetsu Yamanaka, Atsushi Hoshino, Kuniyoshi Fukai, Ryota Urata, Yoshito Minami, Sakiko Honda, Yohei Fushimura, Daichi Hato, Eri Iwai‐Kanai, Satoaki Matoba
Abstract
Pulmonary arterial hypertension is a refractory disease. TP53-induced glycolysis and apoptosis regulator (TIGAR) is a downstream target of p53 and exhibits functions inhibiting autophagy and reactive oxygen species (ROS). By using TIGAR-deficient knockout mice and human pulmonary artery smooth muscle cells, we found that TIGAR suppressed the proliferation and migration of PASMCs via inhibiting autophagy and ROS and, therefore, improved hypoxia-induced PH. TIGAR will be a promising therapeutic target for PAH.
Topics & Concepts
AutophagyReactive oxygen speciesApoptosisHypoxia (environmental)Cell biologyRegulatorPulmonary arteryGlycolysisPulmonary hypertensionSmooth muscleCancer researchCellChemistryBiologyOxygenMedicineInternal medicineBiochemistryEnzymeGeneOrganic chemistryPulmonary Hypertension Research and TreatmentsMicroRNA in disease regulationAutophagy in Disease and Therapy