[Corrigendum] High glucose promotes hepatic fibrosis via miR­32/MTA3­mediated epithelial­to­mesenchymal transition.

Subsequently to the publication of this paper, the authors have realized that Fig. 2 was published containing some incorrectly assembled data panels. The E­cadherin control data panel in Fig. 3F was re­used in Fig. 2C; furthermore, the HG / Vimentin data panel in Fig. 4E was re­used in Fig. 2D. The authors have re­examined their original data, and were able to identify that Fig. 2 contained the erroneously assembled data panels. The revised version of Fig. 2, showing the correct E­cadherin control data panel for Fig. 2C and the correct HG / Vimentin data panel for Fig. 2D, is shown below. It was also noted that the white rectangles were not explained in the figure legend; these represent an enlargement of the cells in the E­cad/vimentin panels, and the details are now included in the figure legend (shown in bold). Note that these errors did not significantly affect either the results or the conclusions reported in this paper, and all the authors agree to the publication of this corrigendum. Furthermore, the authors thank the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 3190­3200, 2019; DOI: 10.3892/mmr.2019.9986].

High glucose promotes hepatic fibrosis via miR­32/MTA3­mediated epithelial­to­mesenchymal transition.

Hepatic fibrosis is characterized by the aberrant production and deposition of extracellular matrix (ECM) proteins. Growing evidence indicates that the epithelial­mesenchymal transition serves a crucial role in the progression of liver fibrogenesis. Although a subset of microRNAs (miRNAs or miRs) has recently been identified as essential regulators of the EMT gene expression, studies of the EMT in hyperglycemic­induced liver fibrosis are limited. In the current study, it was observed that high glucose­treated AML12 cells occurred EMT process, and miR­32 expression was markedly increased in the liver tissue of streptozotocin­induced diabetic rats and in high glucose­treated AML12 cells. Additionally, the contribution of the EMT to liver fibrosis by targeting metastasis­associated gene 3 (MTA3) under hyperglycemic conditions was suppressed by AMO­32. The results indicated that miR­32 and MTA3 may be considered as novel drug targets in the prevention and treatment of liver fibrosis under hyperglycemic conditions. These finding improves the understanding of the progression of liver fibrogenesis.

Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts via upregulating metastasis associated protein 3.

Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis via upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.