Correction to ‘Sirtuin 3 Is Essential for Hypertension-Induced Cardiac Fibrosis via Mediating Pericyte Transition’

IF 4.7

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2026-10-03 DOI:10.1111/jcmm.71388

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Abstract

Su, H, Zeng, H, Liu, B, Chen, J-X. Sirtuin 3 Is Essential for Hypertension-Induced Cardiac Fibrosis via Mediating Pericyte Transition. Journal of Cellular and Molecular Medicine 2020; 24: 8057–8068. https://doi.org/10.1111/jcmm.15437

In Figure 6A of the DHE-stained image for the control WT group, the image was incorrect. The correct image is shown below.

In Figure 5A, the same GAPDH band as in Figure 2D was used, as TGF-β1 and β-MHC were from the same PVDF membrane and shared the same GAPDH band.

Figure 5A and 5B (NG2-DsRed mice). (A) Low-magnification (20X) overview showing the regional expression profile of TGF-β1 (green); the co-stained cell marker channel is omitted here for visual clarity of overall expression levels. (B) High-magnification (40X) individual channels and merged view of the identical tissue section, demonstrating co-localization of TGF-β1 (green) with NG2-DsRed (red) to identify the cell source. The bounding box indicates the region magnified in Panel B.

We apologize for this error.

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修正“Sirtuin 3通过介导周细胞转化对高血压诱导的心脏纤维化至关重要”。

苏慧，曾慧，刘斌，陈建新。Sirtuin 3通过介导周细胞转化对高血压诱导的心脏纤维化至关重要。细胞与分子医学杂志2020；24: 8057 - 8068。https://doi.org/10.1111/jcmm.15437在WT对照组的dhe染色图像的图6A中，图像是错误的。正确的图像如下所示。图5A采用与图2D相同的GAPDH带，因为TGF-β1和β-MHC来自同一PVDF膜，共用同一个GAPDH带。图5A和5B （NG2-DsRed小鼠）。(A)低倍（20倍）全景图，显示TGF-β1的区域表达谱（绿色）；为了整体表达水平的视觉清晰度，这里省略了共染色的细胞标记通道。(B)高倍（40倍）单个通道和同一组织切片的合并视图，显示TGF-β1（绿色）与NG2-DsRed（红色）共定位，以确定细胞来源。边界框表示面板b中放大的区域。我们为这个错误道歉。

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来源期刊

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

CiteScore

11.50

自引率

0.00%

发文量

期刊介绍： The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.