Fig. 3

Participation of SUMOylation in molecular signalling pathways involved in cardiac hypertrophy. SUMO conjugation of Cn facilitated NFAT mediated hypertrophy, while SUMO binding to Myocardin could be a direct hypertrophic stimulus. Likewise, SUMOylated Myom1 can cause sarcomeric reorganization and SUMOylated Drp1 can cause mitochondrial disfunction, both leading to cardiac hypertrophy. These portray SUMO as a foe. But, ZAK, which mediates hypertrophy via c-JUN/GATA and HSP, which causes IGFIIR mediated hypertrophy, both upon SUMO conjugation obstructs their hypertrophic role, attesting SUMO as a friend here. Cn calcineurin, Drp1 dynamin related protein 1, ERβ oestrogen receptor β, HSP2 heat shock protein 2, IGFIIR Insulin growth factor 2 receptor, MAPL mitochondrial anchored protein ligase, Mfn2 mitochondrial fusion protein2, Myom1 myomesin 1, NFAT nuclear factor of activated T cells, PE phenylephrine, PIAS1 protein inhibitor of activated STAT; SENP1 sentrin/SUMO-specific proteases, SUMO2 small ubiquitin related modifier, ZAK sterile alpha motif and leucine zipper containing kinase