炎症
吞噬作用
生物
死孢子体1
纤维化
细胞生物学
免疫学
癌症研究
细胞凋亡
自噬
医学
病理
生物化学
作者
Alissa Gruenwald,Margarete Neururer,Sylvia Eidenhammer,Andreas Nerlich,Helmut Popper
标识
DOI:10.1016/j.prp.2024.155432
摘要
Usual Interstitial Pneumonia (UIP) a fibrosing pneumonia is associated with idiopathic pulmonary fibrosis, chronic autoimmune disease (AID), or hypersensitivity pneumonia. Oxygen radicals, due to tobacco smoke, can damage DNA and might upregulate PARP1. Cytosolic DNA from dying pneumocytes activate cytosolic GMP-AMP-synthase-stimulator of interferon genes (cGAS-STING) pathway and TREX1. Prolonged inflammation induces senescence, which might be inhibited by phagocytosis, eliminating nuclear debris. We aimed to evaluate activation of cGAS-STING-TREX1 pathway in UIP, and if phagocytosis and anti-phagocytosis might counteract inflammation.
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