ArticleActa cirurgica brasileira2019
The liver injury following ischemia and reperfusion is worse in experimental knockout heterozygote mouse model for expression of connexin 431.
Article in Acta cirurgica brasileira, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Ion channel gene signature for diagnosis and antifibrotic therapy in liver fibrosis.Journal of translational medicine · 2026Article
- Intercellular Transmission of Hepatic ER Stress in Obesity Disrupts Systemic Metabolism.Cell metabolism · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
purposeTo evaluate that Connexin (Cx43) plays a role in lesions after hepatic ischemia/reperfusion (IR) injury.
methodsWe 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.
resultsThe 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.
conclusionsThis 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.
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