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Preclinical study demonstrates that TIGAR suppresses smooth muscle cell proliferation and improves hypoxia-induced pulmonary hypertension, highlighting a potential therapeutic target.
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.
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Yamanaka et al. (2020) studied this question.
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