Read the full paper: Efficacy of Retigabine in Treating Weakness in a Mouse Model of Hypokalemic Periodic Paralysis

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The Kv7 (KCNQ) K+ channels family controls neuron excitability, making them significant targets in pain management. This study aims to investigate the potential role of Kv7.2 (KCNQ2) in regulating…

Chronic intermittent hypoxia increases the expression of Hif1α, and Hif1α promotes autophagy activation in hepatocytes, which accelerates the autophagic degradation of Eepd1, a DNA repair enzyme, and hence exacerbates DNA damage in hepatocytes. The increased DNA damage exacerbates liver inflammation, fibrosis, and NASH progression. Eepd1 liver-specific knockout mice aggravate DNA damage and then exacerbate liver inflammation, fibrosis, and NASH progression. Retigabine dihydrochloride, targeting CIH-mediated Eepd1 degradation, can represent an effective treatment for CIH-induced NASH. Abstract Obstructive sleep apnea syndrome (OSAS), characterized by chronic intermittent hypoxia (CIH), is an independent risk factor for aggravating non-alcoholic steatohepatitis (NASH). The prevailing mouse model employed in CIH research is inadequate for the comprehensive exploration of the impact of CIH on NASH development due to reduced food intake observed in CIH-exposed mice, which deviates from human responses. To address this issue, a pair-feeding investigation with CIH-exposed and normoxia-exposed mice is conducted. It is revealed that CIH exposure aggravates DNA damage, leading to hepatic fibrosis and inflammation. The analysis of genome-wide association study (GWAS) data also discloses the association between Eepd1, a DNA repair enzyme, and OSAS. Furthermore, it is revealed that CIH triggered selective autophagy, leading to the autophagic degradation of Eepd1, thereby exacerbating DNA damage in hepatocytes. Notably, Eepd1 liver-specific knockout mice exhibit aggravated hepatic DNA damage and further progression of NASH. To identify a therapeutic approach for CIH-induced NASH, a drug screening is conducted and it is found that Retigabine dihydrochloride suppresses CIH-mediated Eepd1 degradation, leading to alleviated DNA damage in hepatocytes. These findings imply that targeting CIH-mediated Eepd1 degradation can be an adjunctive approach in the treatment of NASH exacerbated by OSAS.