Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPTREVISAN, Alexandre MaximilianoCOGLIATI, BrunoHOMEM, Adriana RibeiroALOIAV, Thiago Pinheiro ArraisAQUINO NETO, Nelson deMOREIRA, Jairo MarquesRENO, Leonardo da CruzNAUMANN, Alexandre MoulinGALVAO, Flavio Henrique FerreiraANDRAUS, WellingtonD'ALBUQUERQUE, Luiz Augusto Carneiro2020-03-242020-03-242019ACTA CIRURGICA BRASILEIRA, v.34, n.10, article ID e201901003, 9p, 20190102-8650https://observatorio.fm.usp.br/handle/OPI/35457Purpose: To evaluate that Connexin (Cx43) plays a role in lesions after hepatic ischemia/reperfusion (IR) injury. Methods: We use Cx43 deficient model (heterozygotes mice) and compared to a wild group. The groups underwent 1 hour ischemia and 24 hours reperfusion. The heterozygote genotype was confirmed by PCR. We analyzed the hepatic enzymes (AST, ALT, GGT) and histology. Results: The mice with Cx43 deficiency showed an ALT mean value of 4166 vs. 307 in the control group (p<0.001); AST mean value of 7231 vs. 471 in the control group (p<0.001); GGT mean value of 9.4 vs. 1.7 in the control group (p=0.001); histology showed necrosis and inflammation in the knockout group. Conclusions: This research demonstrated that the deficiency of Cx43 worses the prognosis for liver injury. The topic is a promising target for therapeutics advancements in liver diseases and procedures.engopenAccessGAP junctionsConnexin 43IschemiaReperfusionLiverCell communicationMiceoxidative stressresectionarticleCopyright ACTA CIRURGICA BRASILEIRA10.1590/s0102-865020190100000003Surgery1678-2674