Pimitespib, an HSP90 inhibitor, augments nifuroxazide-induced disruption in the IL-6/STAT3/HIF-1α autocrine loop in rats with bleomycin-challenged lungs: Evolutionary perspective in managing pulmonary fibrosis

El-Kashef, Dalia HYoussef, Mahmoud ENasr, MohamedAlrouji, MohammedAlhajlah, SharifAlOmeirf, OthmanEl Adle Khalaf, NouraAbdel Ghaffar, Dalia MJamil, LubnaAbdel-Nasser, Zeinab MIbrahim, SamarAbdeldaiem, Mahmoud Said IbrahimDonia, Sally SMohammed, Osama AMorsy, Nesreen ElsayedShata, AhmedSaber, Sameh2022-08-032022-08-032022-07-27https://doi.org/10.1016/j.biopha.2022.113487http://repository.msa.edu.eg/xmlui/handle/123456789/5071Idiopathic pulmonary fibrosis is a fatal lung disorder in which the etiology and pathogenesis are still unobvious. Effective treatments are urgently needed considering that lung transplantation is the only treatment that could improve outcomes. This study aimed to investigate the therapeutic significance of the dual administration of pimitespib, an HSP90 inhibitor, and nifuroxazide, a STAT3 inhibitor, against bleomycin-induced pulmonaryen-USBleomycinNifuroxazidePimitespibSTAT3Pimitespib, an HSP90 inhibitor, augments nifuroxazide-induced disruption in the IL-6/STAT3/HIF-1α autocrine loop in rats with bleomycin-challenged lungs: Evolutionary perspective in managing pulmonary fibrosisArticlehttps://doi.org/10.1016/j.biopha.2022.113487