Jun-xiu Lu, Chao Guo, Wen-sheng Ou, Yun Jing, Hui-fang Niu, Ping Song, Quan-zhi Li, Zhan Liu, Jian Xu, Peng Li, Mo-li Zhu, Ya-ling Yin, “Citronellal Prevents Endothelial Dysfunction and Atherosclerosis in Rats,” Journal of Cellular Biochemistry 120, no. 3 (2019); 3790–3800.
In Figure 2, the representative images of Figure 2A have weak typicality.
Replaced Figure 2.
We apologize for this error.
EXPRESSION OF CONCERN: A. A. Bokhari, V. Syed, “Inhibition of Transforming Growth Factor-β (TGF-β) Signaling by Scutellaria baicalensis and Fritillaria cirrhosa Extracts in Endometrial Cancer,” Journal of Cellular Biochemistry 116, no. 8 (2015): 1797–1805, https://doi.org/10.1002/jcb.25138.
This Expression of Concern is for the above article, published online on June 10, 2015 in Wiley Online Library (wileyonlinelibrary.com), and has been published by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.
The Expression of Concern has been published due to concerns raised by a third party regarding duplicated Western blot bands between the Figure 5 Slug and Figure 6 Integrin β3 subpanels. A subsequent investigation by the journal team identified further inconsistencies regarding duplication of the β-actin control bands in Figures 1A and 3A,B. The authors were informed about the concerns but they remained unresponsive. In the absence of a satisfactory explanation and/or the original raw data, the journal team could not verify the authenticity of these figures and could not exclude that these concerns affect the conclusions of the article. Therefore, the journal has decided to issue an Expression of Concern to inform and alert the readers.
RETRACTION: U. K. Misra, F. Wang, and S. V. Pizzo, “Transcription Factor TFII-I Causes Transcriptional Upregulation of GRP78 Synthesis in Prostate Cancer Cells,” Journal of Cellular Biochemistry 106, no. 3 (2009): 381-389, https://doi.org/10.1002/jcb.22016.
The above article, published online on 18 December 2008 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 1A and 3, and within Figure 3. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.
RETRACTION: U. K. Misra and S. V. Pizzo, “Epac1-Induced Cellular Proliferation in Prostate Cancer Cells Is Mediated by B-Raf/ERK and mTOR Signaling Cascades,” Journal of Cellular Biochemistry 108, no. 4 (2009): 998–1011, https://doi.org/10.1002/jcb.22333.
The above article, published online on 1 September 2009 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 2A and 4B, between Figure 3B and 3D, and between Figures 3B and 4C. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.
RETRACTION: U. K. Misra, and S. V. Pizzo, “Activation of Akt/PDK Signaling in Macrophages Upon Binding of Receptor-Recognized Forms of α2-Macroglobulin to Its Cellular Receptor: Effect of Silencing the CREB Gene,” Journal of Cellular Biochemistry 93, no. 5 (2004): 1020–1032, https://doi.org/10.1002/jcb.20233.
The above article, published online on 9 September 2004 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 2A and 5A, within Figure 3 and between Figures 3 and 4B, and between Figures 4A and 6. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.
RETRACTION: U. K. Misra and S. V. Pizzo, “Upregulation of mTORC2 Activation by the Selective Agonist of EPAC, 8-CPT-2Me-cAMP, in Prostate Cancer Cells: Assembly of a Multiprotein Signaling Complex,” Journal of Cellular Biochemistry 113, no. 5 (2011): 1488–1500, https://doi.org/10.1002/jcb.24018.
The above article, published online on 15 December 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 4C and 7B, between Figure 7A and 7B, and within Figure 6C. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.
RETRACTION: U. K. Misra, Y. M. Mowery, G. Gawdi, and S. V. Pizzo, “Loss of Cell Surface TFII-I Promotes Apoptosis in Prostate Cancer Cells Stimulated With Activated α2-Macroglobulin*,” Journal of Cellular Biochemistry 112, no. 6 (2011): 1685–1695, https://doi.org/10.1002/jcb.23083
The above article, published online on 24 February 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, duplication of image elements has been detected between Figures 1A and 3, and within Figure 3. In all instances, these image elements have been used to represent different experimental conditions. An institutional review confirmed the validity of the concerns. Accordingly, the article is retracted as the editors have lost trust in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors have been informed of the decision of retraction.
H. Li, W. Gong, W. Sun, Y. Yao, and Y. Han, “Role of VPS39, a Key Tethering Protein for Endolysosomal Trafficking and Mitochondria-Lysosome Crosstalk, in Health and Disease,” Journal of Cellular Biochemistry 125, no. 11 (2024): e30396, https://doi.org/10.1002/jcb.30396.
In the article, there is an error in the citation numbering starting from the second paragraph of Section 4.1. The reference numbers in the text do not match the final reference list, and similar discrepancies occur in Table 2.
We apologize for this error.
Correction to “Role of VPS39, A Key Tethering Protein for Endolysosomal Trafficking And Mitochondria–Lysosome Crosstalk, in Health and Disease”
The reference numbers in Table 2 have also been corrected in the same way as the text. Each reference number has been increased by 2 to match the correct reference numbers, as follows:
“88” has been changed to “90”; “89” has been changed to “91”; “90” has been changed to “92”; “91” has been changed to “93”; “92” has been changed to “94”; “93” has been changed to “95”; “94” has been changed to “96”; “95” has been changed to “97”; “96” and “97” have been changed to “98” and “99”; “98” has been changed to “100”; “99” has been changed to “101”; “100” and “101” have been changed to “102” and “103”; “102” has been changed to “104”; “102-104” has been changed to “104–106”; “105” has been changed to “107”; “106” has been changed to “108.”
Beta-hydroxybutyrate (BHB), a key ketone body produced during fatty acid metabolism, plays critical roles in various physiological and pathological conditions. Synthesized in the liver through ketogenesis, BHB serves as an essential energy substrate during glucose deprivation, supporting survival by efficiently utilizing fat reserves. It crosses the blood-brain barrier, providing energy for neuronal function, enhancing cognitive processes such as learning and memory, and offering neuroprotection by modulating synaptic plasticity and neurotransmitter levels. BHB's impact extends to cellular pathways, including autophagy, mitochondrial biogenesis, and epigenetic regulation. By modulating autophagy, BHB ensures mitochondrial integrity and function through intricate molecular pathways involving AMPK, mTOR, PINK1/Parkin, and others. This regulation plays vital roles in neurodegenerative diseases, metabolic disorders, cancer, and cardiovascular diseases, reducing oxidative stress and preventing cellular dysfunction. Epigenetically, BHB acts as an endogenous histone deacetylase inhibitor, inducing beneficial histone modifications that enhance cellular resilience and stress responses. This epigenetic influence is crucial in conditions like diabetes and cancer, aiding insulin secretion, protecting pancreatic beta cells, and impacting cancer cell gene expression and survival. Furthermore, BHB's therapeutic potential is evident in its ability to improve mitochondrial function across various tissues, including neurons, muscle, and liver. By enhancing mitochondrial respiration, reducing oxidative stress, and altering metabolic pathways, BHB mitigates conditions such as ICU-acquired weakness, nonalcoholic fatty liver disease, and cardiovascular diseases. BHB's modulation of autophagy and epigenetic regulation underscores its comprehensive role in cellular homeostasis and health across multiple physiological contexts, providing a foundation for future therapeutic strategies.
The thermogenic capacity of brown adipose tissue (BAT) has garnered much attention for its potential to regulate systemic energy balance. BAT depot size and function need to be tightly regulated to prevent loss of metabolic homeostasis due to energy dissipation via non-shivering thermogenesis. While adipocyte-intrinsic mechanisms controlling thermogenesis are critical, an increasing appreciation for the role of the BAT microenvironment is emerging. For example, changes in circulating hexoses due to dietary intake have shown to impact BAT function. Here, we show that murine BAT preadipocytes metabolism is impacted when fructose is used as the sole carbon source. Similarly, differentiation medium containing only fructose yield mature adipocytes with fewer lipid droplets, with a concomitant decrease in adipogenic genes. These deficiencies are also observed in human BAT preadipocytes, where cutting-edge optical imaging modalities show a decrease in total cell mass and lipid mass in fructose-only medium. Taken together, the metabolic microenvironment significantly impacts BAT growth and function, with implications for the role of diets potentially mitigating the efficacy of BAT-targeted therapies.
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