“…In addition, also other transcription factors (e.g., FOXO3A, NF-kB, p53, and PGC-1α) and signaling components (e.g., c-Jun N-terminal kinase, protein tyrosine phosphatases, cysteine protease Atg4, the mitochondrial peroxiredoxins, the NLRP3 inflammasome, etc.) have been identified as targets of mitochondrial H 2 O 2 (Chandel et al, 2000a,b;Nemoto et al, 2000;Valle et al, 2005;Scherz-Shouval et al, 2007;Chiribau et al, 2008;Cox et al, 2010;Zhou et al, 2011;Chae et al, 2013;Frijhoff et al, 2014;Long et al, 2014;Marinho et al, 2014). However, although it is well known that H 2 O 2 can selectively modify proteins containing cysteine residues with a low pKa (Veal et al, 2007), the precise mechanisms by which mitochondria-derived H 2 O 2 coordinates or relays (retrograde) signaling events thereby provoking adaptive or maladaptive responses are not yet entirely clear (Forkink et al, 2010).…”