International Journal of Biochemistry & Cell Biology最新文献

{"title":"Iron overload increases the sensitivity of endometriosis stromal cells to ferroptosis via a PRC2-independent function of EZH2","authors":"Yong Luo ,&nbsp;Liping Li ,&nbsp;Qiwen Hu ,&nbsp;Ziyu Zhang ,&nbsp;Faying Liu ,&nbsp;Yongbao Peng ,&nbsp;Yang Zou ,&nbsp;Lina Chen","doi":"10.1016/j.biocel.2024.106553","DOIUrl":"10.1016/j.biocel.2024.106553","url":null,"abstract":"<div><p>Given the high concentration of iron in the micro-environment of ovarian endometriosis, it is plausible to hypothesize that ectopic endometrial cells may be more susceptible to undergoing ferroptosis. Manipulation of ferroptosis has been explored as a potential therapeutic strategy to treat related diseases. In this study, we examined the impact on ectopic endometrial stromal cells (EESCs) of iron overload and an inducer of ferroptosis. We found that the iron concentration in the ovarian endometriosis was much higher than control samples. Treatment of cultured EESCs with ferric ammonium citrate (FAC) increase the sensitivity to undergo ferroptosis. By analyzing the RNA-seq results, it was discovered that zeste 2 polycomb repressive complex 2 subunit (EZH2) was significantly downregulated in ferroptosis induced EESCs. Moreover, overexpression of EZH2 effectively prevented the induction of ferroptosis. In addition, the activity or expression of EZH2 is directly and specifically inhibited by the methyltransferase inhibitor GSK343, which raises the sensitivity of stromal cells to ferroptosis. Taken together, our findings revealed that EZH2 act as a suppressor in the induced cell ferroptosis through a PRC2-independent methyltransferase mechanism. Therefore, blocking EZH2 expression and inducing ferroptosis may be effective treatment approaches for ovarian endometriosis.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106553"},"PeriodicalIF":4.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139991713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The application of brain organoid for drug discovery in mitochondrial diseases","authors":"Kristina Xiao Liang","doi":"10.1016/j.biocel.2024.106556","DOIUrl":"10.1016/j.biocel.2024.106556","url":null,"abstract":"<div><p>Mitochondrial diseases are difficult to treat due to the complexity and multifaceted nature of mitochondrial dysfunction. Brain organoids are three-dimensional (3D) structures derived from human pluripotent stem cells designed to mimic brain-like development and function. Brain organoids have received a lot of attention in recent years as powerful tools for modeling human diseases, brain development, and drug screening. Screening compounds for mitochondrial diseases using brain organoids could provide a more physiologically relevant platform for drug discovery. Brain organoids offer the possibility of personalized medicine because they can be derived from patient-specific cells, allowing testing of drugs tailored to specific genetic mutations. In this article, we highlight how brain organoids offer a promising avenue for screening compounds for mitochondrial diseases and address the challenges and limitations associated with their use. We hope this review will provide new insights into the further progress of brain organoids for mitochondrial screening studies.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"170 ","pages":"Article 106556"},"PeriodicalIF":4.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524000475/pdfft?md5=9790abff186a345b881ed118a4959d01&pid=1-s2.0-S1357272524000475-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139998138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLA inhibits TNF-α-induced PANoptosis of prostate cancer cells through metabolic reprogramming","authors":"Yinghui Hao ,&nbsp;Fangmei Xie ,&nbsp;Jieyi He ,&nbsp;Chenqiong Gu ,&nbsp;Ying Zhao ,&nbsp;Wenfeng Luo ,&nbsp;Xiaoyu Song ,&nbsp;Jian Shen ,&nbsp;Li Yu ,&nbsp;Zeping Han ,&nbsp;Jinhua He","doi":"10.1016/j.biocel.2024.106554","DOIUrl":"10.1016/j.biocel.2024.106554","url":null,"abstract":"<div><p>Previous studies have shown that phenyllactic acid (alpha-Hydroxyhydrocinnamic acid, 2-Hydroxy-3-phenylpropionic acid, PLA), a type of organic acid metabolite, has excellent diagnostic efficacy when used to differentiate between prostate cancer, benign prostatic hyperplasia, and prostatitis. This research aims to explore the molecular mechanism by which PLA influences the PANoptosis of prostate cancer (PCa) cell lines. First, we found that PLA was detected in all prostate cancer cell lines (PC-3, PC-3 M, DU145, LNCAP). Further experiments showed that the addition of PLA to prostate cancer cells could promote ATP generation, enhance cysteine desulfurase (NFS1) expression, and reduce tumor necrosis factor alpha (TNF-α) levels, thereby inhibiting apoptosis in prostate cancer cells. Notably, overexpression of NFS1 can inhibit the binding of TNF-α to serpin mRNA binding protein 1 (SERBP1), suggesting that NFS1 competes with TNF-α for binding to SERBP1. Knockdown of SERBP1 significantly reduced the level of small ubiquity-related modifier (SUMO) modification of TNF-α. This suggests that NFS1 reduces the SUMO modification of TNF-α by competing with SERBP1, thereby reducing the expression and stability of TNF-α and ultimately inhibiting apoptosis in prostate cancer cell lines. In conclusion, PLA inhibits TNF-α induced panapoptosis of prostate cancer cells through metabolic reprogramming, providing a new idea for targeted treatment of prostate cancer.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106554"},"PeriodicalIF":4.0,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139974272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of LINC01322 as a potential prognostic biomarker and oncogene promoting tumor progression in lung adenocarcinoma","authors":"Lizhong Zeng ,&nbsp;Ke Mi ,&nbsp;Lei Peng ,&nbsp;Haimei Wen ,&nbsp;Ting Jiao ,&nbsp;Xin Lyu ,&nbsp;Tong Jiao ,&nbsp;Yang Chen ,&nbsp;Jingyan Yuan ,&nbsp;Long Zhang ,&nbsp;Shuanying Yang","doi":"10.1016/j.biocel.2024.106552","DOIUrl":"10.1016/j.biocel.2024.106552","url":null,"abstract":"<div><p>Our study identified a novel long noncoding RNA, LINC01322, that acts as an oncogene in lung adenocarcinoma progression. Cytoplasmic and nuclear RNA purification assays indicated that LINC01322 was localized in the cytoplasm and nucleus. Gene set enrichment analysis revealed the involvement of LINC01322 in the regulation of cell proliferation, migration, and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. LINC01322 may promote lung adenocarcinoma proliferation and migration through the Janus kinase/signal transducer and activator of transcription signaling pathway. <em>In vitro</em> experiments demonstrated that the knockdown of LINC01322 significantly suppressed lung adenocarcinoma cell proliferation, migration, and activation of the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway, whereas overexpression had the opposite effects. Inhibition of the Janus kinase 2/signal transducer and activator of transcription 3 pathway activity partially reversed the enhancement of cell proliferation and migration caused by LINC01322 overexpression. <em>In vivo</em> experiments further verified the oncogene role of LINC01322. Altogether, our findings suggest that LINC01322 promotes lung adenocarcinoma progression by activating the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway and that it could be a therapeutic target.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106552"},"PeriodicalIF":4.0,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139974271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S100A4 modulates cell proliferation, apoptosis and fibrosis in the hyperplastic prostate","authors":"Liang Yang ,&nbsp;Jiang Liu ,&nbsp;Jing Yin ,&nbsp;Yan Li ,&nbsp;Jianmin Liu ,&nbsp;Daoquan Liu ,&nbsp;Zhen Wang ,&nbsp;Michael E. DiSanto ,&nbsp;Xinhua Zhang ,&nbsp;Weibing Zhang","doi":"10.1016/j.biocel.2024.106551","DOIUrl":"10.1016/j.biocel.2024.106551","url":null,"abstract":"<div><p>Benign prostatic hyperplasia (BPH) is one of the most common diseases in elderly men worldwide that may result in lower urinary tract symptoms (LUTS). At present, the specific pathophysiological mechanism for BPH/LUTS LUTS remains unclear. S100 calcium binding protein A4 (S100A4), a member of the calcium binding protein family, regulates a variety of biological processes including cell proliferation, apoptosis and fibrosis. The aim of the current study was to explore and clarify the possible role of S100A4 in BPH/LUTS. The human prostate stromal cell line (WPMY-1), rat prostate epithelial cells, human prostate tissues and two BPH rat models were employed in this study. The expression and localization of S100A4 were detected by quantitative real time PCR (qRT-PCR), immunofluorescence microscopy, Western blotting and immunohistochemistry analysis. Also, S100A4 knockdown or overexpression cell models were constructed and a BPH rat model was induced with testosterone propionate (T) or phenylephrine (PE). The BPH animals were treated with Niclosamide, a S100A4 transcription inhibitor. Results demonstrated that S100A4 was mainly localized in human prostatic stroma and rat prostatic epithelium, and showed a higher expression in BPH. Knockdown of S100A4 induced cell apoptosis, cell proliferation arrest and a reduction of tissue fibrosis markers. Overexpression of S100A4 reversed the aforementioned changes. We also demonstrated that S100A4 regulated proliferation and apoptosis mainly through the ERK pathway and modulated fibrosis <em>via</em> Wnt/β-catenin signaling. In conclusion, our novel data demonstrate that S100A4 could play a crucial role in BPH development and may be explored as a new therapeutic target of BPH.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106551"},"PeriodicalIF":4.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139742582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The functional significance of circRNA/miRNA/mRNA interactions as a regulatory network in lung cancer biology","authors":"Shengnan Jia ,&nbsp;Ling Yu ,&nbsp;Lihui Wang ,&nbsp;Liping Peng","doi":"10.1016/j.biocel.2024.106548","DOIUrl":"10.1016/j.biocel.2024.106548","url":null,"abstract":"<div><p>Lung cancer, the leading cause of cancer-related deaths, presents significant challenges to patients due to its poor prognosis. Recent research has increasingly implicated circular RNAs in the development and progression of lung cancer. These circular RNAs have been found to impact various aspects of tumor behavior, including proliferation, metastasis, cell cycle regulation, apoptosis, cancer stem cells, therapy response, and the tumor microenvironment. One of the key mechanisms by which circular RNAs exert their influence is through their ability to act as miRNA sponges, sequestering microRNAs and preventing them from targeting other RNA molecules. Accumulating evidence suggests that circular RNAs can function as competing endogenous RNAs, affecting the expression of target mRNAs by sequestering microRNAs. Dysregulation of competing endogenous RNAs networks involving circular RNAs, microRNAs, and mRNAs leads to the aberrant expression of oncogenes and tumor suppressors involved in lung cancer pathogenesis. Understanding the dynamic interplay and molecular mechanisms among circular RNAs, microRNAs, and mRNAs holds great promise for advancing early diagnosis, personalized therapeutic interventions, and improved patient outcomes in lung cancer. Therefore, this study aims to provide an in-depth exploration of the executive roles of circular RNAs/microRNAs/ mRNAs interactions in lung cancer pathogenesis and their potential utility for diagnosing lung cancer, predicting patient prognosis, and guiding targeted therapies. By offering a comprehensive overview of the dysregulation of the axes as driving factors in lung cancer, we aim to pave the way for their translation into clinical practice in the future.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106548"},"PeriodicalIF":4.0,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139742583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of PKM2 as a pyroptosis-related key gene aggravates senile osteoporosis via the NLRP3/Caspase-1/GSDMD signaling pathway","authors":"Zilin Li ,&nbsp;Bo Wang ,&nbsp;Ruoyu Wang ,&nbsp;Zhichao Zhang ,&nbsp;Jian Xiong ,&nbsp;Xiaoyun Wang ,&nbsp;Yan Ma ,&nbsp;Lizhi Han","doi":"10.1016/j.biocel.2024.106537","DOIUrl":"10.1016/j.biocel.2024.106537","url":null,"abstract":"<div><h3>Backgrounds</h3><p>Senile osteoporosis—alternatively labeled as skeletal aging—encompasses age-induced bone deterioration and loss of bone microarchitecture. Recent studies have indicated a potential association between senile osteoporosis and chronic systemic inflammation, and pyroptosis in bone marrow-derived mesenchymal stem cells is speculated to contribute to bone loss and osteoporosis. Therefore, targeting pyroptosis in stem cells may be a potential therapeutic strategy for treating osteoporosis.</p></div><div><h3>Methods</h3><p>Initially, we conducted bioinformatics analysis to screen the GEO databases to identify the key gene associated with pyroptosis in senile osteoporosis. Next, we analyzed the relationship between altered proteins and clinical data. <em>In vitro</em> experiments were then performed to explore whether the downregulation of PKM2 expression could inhibit pyroptosis. Additionally, an aging-related mouse model of osteoporosis was established to validate the efficacy of a PKM2 inhibitor in alleviating osteoporosis progression.</p></div><div><h3>Results</h3><p>We identified PKM2 as a key gene implicated in pyroptosis in senile osteoporosis patients through bioinformatics analysis. Further analyses of bone marrow and stem cells demonstrated significant PKM2 overexpression in senile osteoporosis patients. Silencing PKM2 expression inhibited pyroptosis in senile stem cells, of which the osteogenesis potential and angiogenic function were also primarily promoted. Moreover, the results in vivo demonstrated that administering PKM2 inhibitors suppressed pyroptosis in senile osteoporosis mice and mitigated senile osteoporosis progression.</p></div><div><h3>Conclusion</h3><p>Our study uncovered PKM2, a key pyroptosis marker of bone marrow mesenchymal stem cells in senile osteoporosis. Shikonin, a PKM2 inhibitor, was then identified as a potential drug candidate for the treatment of osteoporosis.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106537"},"PeriodicalIF":4.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139718031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xuetongsu attenuates bone destruction in collagen-induced arthritis mice by inhibiting osteoclast differentiation and promoting osteoclast apoptosis","authors":"Hao Zheng ,&nbsp;Yunzhe Li ,&nbsp;Yasi Deng,&nbsp;Huanjie Li,&nbsp;Xinyang Shen,&nbsp;Haokai Lin,&nbsp;Yong Yang,&nbsp;Xing Tian,&nbsp;Bin Li,&nbsp;Hanwen Yuan,&nbsp;Wenbing Sheng,&nbsp;Wei Wang,&nbsp;Huanghe Yu","doi":"10.1016/j.biocel.2024.106550","DOIUrl":"10.1016/j.biocel.2024.106550","url":null,"abstract":"<div><p>Tujia ethnomedicine Xuetong (the stems of <em>Kadsura heteroclita</em>) have been widely used in folk for rheumatoid arthritis (RA), which can alleviate rheumatic pain through liquor soaking in folk. In this study, we aimed to evaluate the pharmacological effects and underlying mechanism of Xuetongsu (a key chemical component of Xuetong) on bone destruction. In our previous study, it was found that Xuetong extract can reduce adjuvant arthritic rats paw swelling and inhibit inflammatory factors in serum. Furthermore, Xuetongsu has been demonstrated to inhibit the proliferation of fibroblast-like synoviocytes, but its potential to inhibit bone destruction has not been explored. To address this, we employed the STRING database to predict protein interactions and utilized Autodock software to simulate the binding of Xuetongsu to target proteins. In this study, administration of Xuetongsu significantly alleviated paw swelling and bone destruction in C57BL/6 mice with collagen-induced arthritis (CIA). Mechanistic studies have indicated that Xuetongsu promotes apoptosis of mature osteoclasts in joint tissues by activating Caspase-3 and Bax, while inhibiting Bcl-2. Additionally, Xuetongsu inhibits osteoclast differentiation by suppressing RANKL, RANK, <em>P</em>-NF-κB, and NFATc1, and reduces bone resorption activity by inhibiting MMP-9, CTSK, and TRAP. Importantly, Xuetongsu exhibits good biocompatibility in major organs of mice. In summary, Xuetongsu has the potential to treat bone destruction by promoting apoptosis of mature osteoclasts, inhibiting osteoclast differentiation, and reducing bone resorption. This study reveals the pharmacological effects of Xuetongsu and its mechanism of action, which may contribute to the development of novel approaches for treating RA.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106550"},"PeriodicalIF":4.0,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139716580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Herb pair of Rhubarb-Astragalus mitigates renal interstitial fibrosis through downregulation of autophagy via p38-MAPK/TGF-β1 and p38-MAPK/smad2/3 pathways","authors":"Jinxiu Li ,&nbsp;Xiping Qin ,&nbsp;Weimin Xu ,&nbsp;Hongliang Zhang ,&nbsp;Songqing Huang ,&nbsp;Yufang Yang ,&nbsp;Mengyuan Qin ,&nbsp;Zhengcheng Mi ,&nbsp;Xiaobin Zhong","doi":"10.1016/j.biocel.2024.106549","DOIUrl":"10.1016/j.biocel.2024.106549","url":null,"abstract":"<div><h3>Background</h3><p>Chronic kidney disease (CKD) has a high incidence and poor prognosis; however, no effective treatment is currently available. Our previous study found that the improvement effect of the herb pair of Rhubarb-Astragalus on CKD is likely related to the inhibition of the TGF-β1/p38-MAPK pathway. In the present study, a p38-MAPK inhibitor was used to further investigate the inhibitory effect of Rhubarb-Astragalus on the TGF-β1/p38-MAPK pathway and its relationship with autophagy.</p></div><div><h3>Methods</h3><p>A rat model of unilateral ureteral obstruction (UUO) was established, and a subgroup of rats was administered Rhubarb-Astragalus. Renal function and renal interstitial fibrosis (RIF) were assessed 21 d after UUO induction. <em>In vitro</em>, HK-2 cells were treated with TGF-β1 and a subset of cells were treated with Rhubarb-Astragalus or p38-MAPK inhibitor. Western blotting, immunohistochemistry, and qRT-PCR analyses were used to detect the relevant protein and mRNA levels. Transmission electron microscopy was used to observe autophagosomes.</p></div><div><h3>Results</h3><p>Rhubarb-Astragalus treatment markedly decreased the elevated levels of blood urea nitrogen, serum creatinine, and urinary N-acetyl-β-D-glucosaminidase; attenuated renal damage and RIF induced by UUO; and reduced the number of autophagosomes and lysosomes in UUO-induced renal tissues. Additionally, Rhubarb-Astragalus reduced the protein and mRNA levels of α-SMA, collagen I, LC3, Atg3, TGF-β1, p38-MAPK, smad2/3, and TAK1 in renal tissues of UUO rats. Rhubarb-Astragalus also reduced protein and mRNA levels of these indicators in vitro. Importantly, the effect of the p38-MAPK inhibitor was similar to that of Rhubarb-Astragalus.</p></div><div><h3>Conclusions</h3><p>Rhubarb-Astragalus improves CKD possibly by downregulating autophagy via the p38-MAPK/TGF-β1 and p38-MAPK/smad2/3 pathways.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106549"},"PeriodicalIF":4.0,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139716579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Anti-inflammatory actions of (-)-epicatechin in the adipose tissue of obese mice” [Int. J. Biochem Cell Biol. 81 (2016) 383–392]","authors":"Ahmed Bettaieb ,&nbsp;Eleonora Cremonini ,&nbsp;Heeteak Kang ,&nbsp;Jiye Kang ,&nbsp;Fawaz G. Haj ,&nbsp;Patricia I. Oteiza","doi":"10.1016/j.biocel.2024.106534","DOIUrl":"10.1016/j.biocel.2024.106534","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"169 ","pages":"Article 106534"},"PeriodicalIF":4.0,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524000256/pdfft?md5=e3098cf7321ebd4100297faeeb65cd46&pid=1-s2.0-S1357272524000256-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139708410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}