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. 2021 Apr 21;73(3):712–727. doi: 10.1007/s43440-021-00255-x

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© Maj Institute of Pharmacology Polish Academy of Sciences 2021

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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Fig. 7 — Pirfenidone activates peroxisome proliferator-activated receptors (alpha and gamma) (PPAR) [111, 126]. PPAR activates PPAR response element (PPRE). PPRE increases the activity of heme oxygenase-1 (HO-1) [115]. HO-1 coverts free heme to carbon monoxide (CO), ferrous iron, and biliverdin [116]. CO shows anti-oxidant and anti-inflammatory effects [119, 120]. Biliverdin is converted to bilirubin with the help of biliverdin reductase (BVR) and shows anti-oxidant activity [117]. Furthermore, pirfenidone, by blocking BTB domain and CNC homolog 1 (Bach1) increases the activity of anti-oxidant redox elements (ARE). ARE upregulates the expression of HO-1 and anti-oxidant system. By blocking TGF-β, pirfenidone indirectly activates nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 activates ARE. Pirfenidone indirectly causes the dissociation of Nrf2 from KEAP1. The dissociated KEAP1 inhibits IκB kinase (IKK) and blocks the activity of nuclear factor-kappa (NF-kB) [127–130]