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AIM: This study aims to examine the ependymin-related protein 1 (EPDR1) expression in various tissues from wild-type C57BL/6 mice and type 2 diabetes (db/db) mice. The impact of EPDR1 on lipid accumulation in alpha mouse liver 12 (AML12) hepatocytes was also investigated. METHODS: Western blot was used to detect EPDR1 protein expression in the heart, liver, spleen, lung, kidney, gastrocnemius, brown adipose and brain tissues of C57BL/6 mice. Western blot and immunohistochemical (IHC) staining were also used to compare EPDR1 protein expression in the liver, gastrocnemius muscle, heart and kidney tissues of db/db and C57BL/6 mice. To develop an AML12 cell lipid deposition model, palmitic acid (PA)+oleic acid (OA) was used, and the cells were transfected with adenovirus overexpressing EPDR1 or treated with exogenous recombinant EPDR1 protein (rEPDR1). ELISA was conducted to determine intracellu-lar triglyceride (TG) content, and oil red O staining was employed to assess the effect of EPDR1 on lipid accumulation in AML12 cells. RESULTS: Western blot and IHC staining results revealed that EPDR1 was widely expressed in various tissues of wild-type mice, with the liver exhibiting the highest protein expression level. However, EPDR1 expression was down-regulated in the liver, gastrocnemius muscle, heart and kidney tissues in diabetic db/db mice compared with wild-type mice. Oil red O staining revealed that overexpression of EPDR1 in AML12 liver cells or rEPDR1 treatment led to reduced lipid accumulation. Furthermore, the TG content significantly decreased compared with the model group (P< 0. 05). CONCLUSION: EPDR1 is expressed in various tissues of wild-type mice, but showed diminished expression in the liver tissues of diabetic mice. Nevertheless, enhancing the expression of EPDR1 can aid in reducing lipid accumula tion in hepatocytes. These findings provide an experimental foundation for further exploration of the role of EPDR1 in the development of fatty liver in diabetic liver tissue. [ABSTRACT FROM AUTHOR]

Jiangnan Yu and Hong Yang contributed equally to this work.Correction: BMC Gastroenterol 24, 106 (2024)https://doi.org/10.1186/s12876-024-03195-xFollowing publication of the original article [[1]] it was reported that there was an error with Fig. 2, specifically panel 2F. The image used for Fig. 2F was a repetition of Fig. 3G.The incorrect Fig. 2 is shown below:GraphThe correct Fig. 2 is:GraphThe original article has been updated.By Jiangnan Yu; Hong Yang; Lin Zhang; Suye Ran; Qing Shi; Pailan Peng; Qi Liu and Lingyu SongReported by Author; Author; Author; Author; Author; Author; Author; Author [Extracted from the article]

Aquaporins (AQPs) regulate the transport of water and other substrates, aiding plants in adapting to stressful environments. However, the knowledge of AQPs in salt‐secreting and viviparous Avicennia marina is limited. In this study, 46 AmAQPs were identified in A. marina genome, and their subcellular localisation and function in transporting H2O2 and boron were assessed through bioinformatics analysis and yeast transformation. Through analysing their expression patterns via RNAseq and real‐time quantitative polymerase chain reaction, we found that most AmAQPs were downregulated in response to salt and tidal flooding. AmPIP (1;1, 1;7, 2;8, 2;9) and AmTIP (1;5, 1;6) as salt‐tolerant candidate genes may contribute to salt secretion together with Na+/H+ antiporters. AmPIP2;1 and AmTIP1;5 were upregulated during tidal flooding and may be regulated by anaerobic‐responsive element and ethylene‐responsive element cis‐elements, aiding in adaptation to tidal inundation. Additionally, we found that the loss of the seed desiccation and dormancy‐related TIP3 gene, and the loss of the seed dormancy regulator DOG1 gene, or DOG1 protein lack heme‐binding capacity, may be genetic factors contributing to vivipary. Our findings shed light on the role of AQPs in A. marina adaptation to intertidal environments and their relevance to salt secretion and vivipary. Summary statement: AmAQPs respond to salinity and tidal inundation in Avicennia marina, some of which play a role in salt gland secretion and function as water effluxes. The absence of TIP3, an aquaporin isoform, and the loss of DOG1, or its ability to bind to heme, may be one of the causes of vivipary in mangrove plants. [ABSTRACT FROM AUTHOR]

Chrysanthemum morifolium cv. ‘Huaihuang’ has great medicinal and commercial value. However, limited genomic and transcriptional information restricts the further research of ‘Huaihuang’. In this study, using ‘Huaihuang’ leaf as the sample, we performed RNA-Seq and obtained numerous unigene sequences for functional characterization, and developed new EST-SSR markers. The results show that 176 unigenes were assigned to the ‘antioxidant activity’ in GO annotations, 998 unigenes were assigned to ‘Secondary metabolite biosynthesis, transport and catabolism’ in the KOG database, 381 unigenes were assigned to ‘Biosynthesis of other secondary metabolites’, and 377 unigenes were assigned to ‘Metabolism of terpenoids and polyketides’ in the KEGG database. A number of genes involved in the biosynthesis of flavones and terpenes, such as CHS, CHI, FLS, HMGR and MVD, were found in the transcription data of ‘Huaihuang’. Also, 36 new polymorphic EST-SSR markers were developed and validated. Using them, the genetic diversity was analyzed and a dendrogram of six clades was constructed among 15 medicinal chrysanthemum varieties. The excavated unigenes and identified new ESTSSR markers will provide useful resources for the study of biosynthesis of active components, genetic diversity analysis, population structure identification and in molecular breeding research of ‘Huaihuang’ and related species.

From the perspective of complexity economics, this paper studied the international dry bulk freight rate system, put forward the concept and structure model of the international dry bulk freight rate system and summarized its characteristics such as emergent properties, dynamicity, evolution and innovation, nonlinearity and non-equilibrium, which provides a new idea and research method for the study of the international dry bulk freight rate system.

Ectopic lipid accumulation in renal tubules is closely related to the pathogenesis of diabetic kidney disease (DKD), and mitochondrial dysfunction is thought to play a key role in lipid accumulation. Therefore, maintaining mitochondrial homeostasis holds considerable promise as a therapeutic strategy for the treatment of DKD. Here, we report that the Meteorin-like (Metrnl) gene product mediates lipid accumulation in the kidney and has therapeutic potential for DKD. We confirmed the reduced expression of Metrnl in renal tubules, which was inversely correlated with DKD pathological changes in human patients and mouse models. Functionally, pharmacological administration of recombinant Metrnl (rMetrnl) or Metrnl overexpression could alleviate lipid accumulation and inhibit kidney failure. In vitro, rMetrnl or Metrnl overexpression attenuated palmitic acid–induced mitochondrial dysfunction and lipid accumulation in renal tubules accompanied by maintained mitochondrial homeostasis and enhanced lipid consumption. Conversely, shRNA-mediated Metrnl knockdown diminished the protective effect on the kidney. Mechanistically, these beneficial effects of Metrnl were mediated by the Sirt3-AMPK signaling axis to maintain mitochondrial homeostasis and through Sirt3-uncoupling protein-1 to promote thermogenesis, consequently alleviating lipid accumulation. In conclusion, our study demonstrates that Metrnl regulated lipid metabolism in the kidney by modulating mitochondrial function and is a stress-responsive regulator of kidney pathophysiology, which sheds light on novel strategies for treating DKD and associated kidney diseases. Article Highlights: Metrnl is expressed in renal tubules and is reduced under diabetic conditions. The concentration of Metrnl in the kidney is correlated with lipid accumulation and serum creatinine. Metrnl-specific overexpression in the kidney or recombinant Metrnl administration alleviates renal injuries in diabetic mice. Metrnl regulates renal tubules lipid metabolism through Sirt3-AMPK/UCP1 signaling axis–mediated mitochondrial homeostasis. [ABSTRACT FROM AUTHOR]