In this study, we identified 34 CCCH Znf genes in Medicago truncatula and the results of semi-quantitative RT-PCR revealed that the expression patterns of subfamily VI members were diverse. CCCH-type zinc finger (Znf) proteins are specific transcriptional factors with a typical motif consisting of three cysteine residues and one histidine residue. Increasing evidences have revealed that CCCH Znf proteins participated in the regulation of plant growth, developmental processes and environmental responses. Survey and characterization of CCCH Znf genes in leguminous species would facilitate a better understanding of the evolutionary processes and functions of this gene family. In this study, we performed a comprehensive analysis of CCCH Znf genes in M. truncatula by describing the phylogenetic relationships, chromosomal location and gene structure of each family member. A total of 34 CCCH Znf genes were identified in the latest M. truncatula genome sequence. The 34 predicted members were clustered into nine subfamilies based on their phylogenetic analysis and structure features. In addition, the 34 Medicago CCCH Znf genes were found to be unevenly distributed on eight chromosomes. Furthermore, the expression profiles of subfamily VI were investigated under different stress conditions (PEG-6000, NaCl and ABA) by using semi-quantitative RT-PCR. The data showed that these genes displayed different expression levels in response to various stress conditions. The results presented in this study provide basic information about Medicago CCCH Znf genes and form a fundamental clue for cloning genes with specific functions in further studies and applications.

ALD is prevalent in north-eastern China. SES correlates with the development of ALD. Socioeconomic risk factors for ALD in north-eastern China include male gender, middle age, currently unmarried, low level of education, low family income, and high level of occupation.

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Background Liver fibrosis is a pathological wound-healing response caused by chronic liver damage. Mitochondria regulate hepatic energy metabolism and oxidative stress. Accumulating evidence has revealed that increased mitochondrial oxidative stress contributes to the activation of fibrogenesis. However, the roles and underlying mechanisms of mitochondrial oxidative stress in liver fibrosis remain unknown. Methods and results In this study, C57BL/6 mice were used to establish a model of liver fibrosis via oral gavage with CCl4 treatment for 8 weeks. Furthermore, intervention experiments were achieved by CCl4 combined with the intraperitoneal injection of mitoquinone mesylate (mitoQ). We demonstrated that the chronic CCl4 exposure resulted in severe hepatic fibrogenesis and significantly promoted the production of reactive oxygen species (ROS) and mitochondrial abnormalities. Besides, JNK/YAP pathway was also activated. By contrast, the administration of mitoQ markedly inhibited the expression of pro-fibrogenic transforming growth factor-β as well as type I collagen. The antifibrotic effects of mitoQ were also confirmed by hematoxylin and eosin staining and Sirius red staining. Moreover, mitoQ substantially reduced CCl4-induced mitochondrial damage and the release of ROS. Further studies suggested that this protection against liver fibrosis was mechanistically related to the inhibition of phosphorylation of JNK and the nuclear translocation of YAP. Conclusion In conclusion, these findings revealed that mitoQ attenuated liver fibrosis by inhibiting ROS production and the JNK/YAP signaling pathway. Selective targeting JNK/YAP may serve as a therapeutic strategy for retarding progression of chronic liver disease.