Altered AKAP12 expression in portal fibroblasts and liver sinusoids mediates transition from hepatic fibrogenesis to fibrosis resolution

• Main Authors: Hye Shin Lee, Jinhyeok Choi, Taekwon Son, Hee-Jun Wee, Sung-Jin Bae, Ji Hae Seo, Ji Hyun Park, Soo Hyung Ryu, Danbi Lee, Myoung Kuk Jang, Eunsil Yu, Young-Hwa Chung, Kyu-Won Kim
• Format: Article
• Language: English
• Published: Nature Publishing Group 2018-04-01
• Series: Experimental and Molecular Medicine
• Online Access: https://doi.org/10.1038/s12276-018-0074-5

Liver fibrosis: Reversing the damage A scaffolding protein that modulates cell signaling pathways contributes to reverse liver scarring. Liver fibrosis is caused by a build-up of scar tissue that interferes with liver function. However, the damage is reversed when the cause of injury is removed. Kyu-Won Kim at Seoul National University, South Korea, and colleagues examined the levels of A-Kinase Anchoring Protein 12 (AKAP12), a scaffolding protein that regulates the subcellular location of signaling proteins, in mouse and human livers. Levels of AKAP12 were reduced in fibrotic livers but restored when fibrosis was reversed. Mice lacking AKAP12 were unable to effectively repair the damage caused by fibrosis. Genetic analyses suggest that AKAP12 stimulates signaling through the adenosine 3′,5′-cyclic monophosphate (cAMP) pathway, which can inhibit fibrosis. These findings highlight a key role for AKAP12 in accelerating liver recovery.