Cell Biology International最新文献

{"title":"Regulation of N-Glycosylation of CDNF on Its Protein Stability and Function in Hypoxia/Reoxygenation Model of H9C2 Cells.","authors":"Qingwen Huang, Haibin Dong, Wenjuan Jia, Yanxin Ren, Wei Li, Lin Zhong, Lei Gong, Jun Yang","doi":"10.1002/cbin.70000","DOIUrl":"https://doi.org/10.1002/cbin.70000","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion (I/R) injury is a cause of high post-interventional mortality in patients with acute myocardial infarction (MI). Cerebral dopamine neurotrophic factor (CDNF) is an endoplasmic reticulum (ER) resident protein, and its expression and secretion are induced when tissues and cells are subjected to hypoxia, ischemia, or traumatic injury. As a novel cardiomyokine, CDNF plays a crucial role in the progression of myocardial I/R injury. In our previous study, we reported that the overexpression of CDNF inhibited tunicamycin-induced H9C2 cell apoptosis. Moreover, there is a unique N-glycosylation site at Asn57 in the CDNF protein, which likely affects its function in H9C2 cells. However, the detailed impact remains unexplored. In our current study, we observed elevated levels of CDNF in the serum of acute MI patients, myocardial tissue of I/R model mice, and H/R model H9C2 cells. To detect the effect of N-glycosylation on the CDNF protein, we constructed an Asn57 mutant (N57A) plasmid and found that the N57A protein presented similar intracellular localization to those of the wild-type CDNF protein. However, the N57A protein demonstrated reduced stability, and the mutant protein could not protect H/R-induced H9C2 cells from apoptosis. Moreover, this process may occur through the downregulation of the PI3K/Akt pathway. Therefore, N-glycosylation of CDNF may be essential for protein stability and its protective role in H/R injury in H9C2 cells.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373733","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":"AKR1B1 Inhibits Ferroptosis and Promotes Gastric Cancer Progression via Interacting With STAT3 to Activate SLC7A11","authors":"Kaiyan Yang,&nbsp;Xin Zhang,&nbsp;Fei Long,&nbsp;Jing Dai","doi":"10.1002/cbin.12275","DOIUrl":"10.1002/cbin.12275","url":null,"abstract":"<div>\u0000 \u0000 <p>Gastric cancer (GC) is a frequently diagnosed malignant tumor in clinical settings; however, the mechanisms underlying its tumorigenesis remain inadequately understood. In this study, we identified significantly elevated expression levels of AKR1B1 in GC tissues through quantitative polymerase chain reaction (qPCR) and western blotting assays. Furthermore, a negative correlation was established between patient survival probability and AKR1B1 expression levels. Functionally, our experiments, including colony formation, transwell migration, and xenograft assays, demonstrated that the depletion of AKR1B1 inhibited the proliferation and progression of GC cells both in vivo and in vitro. Additionally, the assessment of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and mitochondrial morphology confirmed that AKR1B1 depletion induces ferroptosis. Mechanistically, we found that AKR1B1 interacts with STAT3, which subsequently activates SLC7A11. Notably, the ferroptosis induced by AKR1B1 depletion could be reversed by the overexpression of SLC7A11, thereby substantiating these interactions. In conclusion, our findings identify AKR1B1 as a novel oncogene in GC and elucidate the mechanism involving the AKR1B1-STAT3-SLC7A11 pathway and ferroptosis, providing new insights for potential therapeutic strategies in the treatment of GC.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"374-383"},"PeriodicalIF":3.3,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254774","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":"TREM2 as a Therapeutic Target in Atherosclerosis","authors":"Siting Xu,&nbsp;Bo Yang,&nbsp;Wenhua Yu,&nbsp;Yun Gao,&nbsp;Honghua Cai,&nbsp;Zhongqun Wang","doi":"10.1002/cbin.12279","DOIUrl":"10.1002/cbin.12279","url":null,"abstract":"<div>\u0000 \u0000 <p>Atherosclerosis is driven by the expansion of cholesterol-loaded foamy macrophages in the arterial intima. Single-cell RNA sequencing has recently revealed the transcriptional landscape of macrophages in these atherosclerotic plaques and uncovered a population of foamy cell-like myeloid cells expressing triggering receptor expressed on myeloid cells-2 (TREM2)—TREM2^hi macrophages. Fundamental research has brought essential insight into the significance of TREM2 for foam macrophage survival and atherosclerosis progression, making TREM2 as a therapeutic target in atherosclerosis possible. This review retraces TREM2's winding route from pure knowledge to therapeutic interventions, as well as the potential feasibility of its clinical application for atherosclerosis.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"305-316"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073934","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":"PRMT5 Inhibition Enhances Therapeutic Efficacy of Cisplatin via Mediating miR-29b-3p-Mcl-1 Expression in Lung Adenocarcinoma","authors":"Haichao Li,&nbsp;Jiangjiang Fan,&nbsp;Weiwei Shen,&nbsp;Yong Zhang,&nbsp;Ximing Zhu,&nbsp;Pei Li,&nbsp;Zhongping Gu,&nbsp;Pengyu Jing","doi":"10.1002/cbin.12278","DOIUrl":"10.1002/cbin.12278","url":null,"abstract":"<div>\u0000 \u0000 <p>Cisplatin is one of the front-line therapeutic agents used to treat cancers, while drug resistance is a great obstacle to anti-tumor efficiency. Protein arginine methyltransferase 5 (PRMT5) has been identified as a promoter of tumorigenesis, motility, and invasion. Inhibiting PRMT5 reduced hypoxia-induced carboplatin resistance in lung adenocarcinoma (LUAD). However, the specific relationship between PRMT5 and cisplatin (CDDP) warrants further investigation. Our research revealed that PRMT5 inhibitor C9 enhanced CDDP chemosensitivity by suppressing proliferation and promoting apoptosis in LUAD cells. Through examining pro-apoptotic proteins regulated by PRMT5, we identified that Mcl-1 played a significant role in PRMT5-mediated CDDP chemosensitivity. Furthermore, PRMT5 regulated Mcl-1 expression through mediating miR-29b-3p. In vivo, our research presented that C9 increased CDDP chemosensitivity in LUAD xenografts. All in all, our data raised an interesting possibility that epigenetic reprogramming was associated with chemosensitivity. PRMT5 inhibitor C9 improved CDDP effectiveness in LUAD cells by inhibiting Mcl-1 expression via miR-29b-3p, thereby modulating cellular proliferation and apoptosis.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"407-418"},"PeriodicalIF":3.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073933","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":"Anticancer Attributes and Multifaceted Pharmacological Implications of Laetrile and Amygdalin","authors":"Katya Carbone,&nbsp;Oksana Sytar,&nbsp;Farukh Sharopov,&nbsp;Raffaele Pezzani,&nbsp;Raffaele Romano,&nbsp;Antonello Santini,&nbsp;Marek Kieliszek,&nbsp;Tooba Khan,&nbsp;Khushbukhat Khan,&nbsp;Angela Caunii,&nbsp;Solomon Habtemariam,&nbsp;Javad Sharifi-Rad,&nbsp;Monica Butnariu","doi":"10.1002/cbin.12276","DOIUrl":"10.1002/cbin.12276","url":null,"abstract":"<div>\u0000 \u0000 <p>Laetrile, known as vitamin B17, is often used interchangeably with amygdalin. Laetrile is a semi-synthesis product of amygdalin, whereas amygdalin is a naturally occurring substance in many plants. Both compounds have a nitrile functional group that, when activated by the intestinal enzyme β-glucosidases, releases hydrogen cyanide. The two compounds have been considered for a long time as alternative therapy for cancer treatment however, findings available in the literature are discordant on the real efficacy of laetrile/amygdalin for the treatment of cancer, often highlighting a negative benefit-risk ratio. In this regard, the study aimed to comprehensively analyze the scientific data on laetrile/amygdalin, with a special emphasis on their pharmacokinetics, underlying pharmacological properties, mode of action as a potent antitumor agent, and effect on human health. The results showed that there is no clear evidence on the efficacy of cancer therapy following laetrile/amygdalin administration, especially at the clinical trial level. However, the in vitro studies of the biological activity of these compounds showed positive effects related to their antifibrotic, anti-inflammatory, antiasthmatic, and immunoregulatory processes. Laetrile's mechanism of action closely resembles amygdalin, affecting cancer signaling pathways. However, due to its cyanide toxicity, it was banned by the food and drug administration (FDA) due to safety concerns. Despite not receiving permission from the FDA, laetrile emerged as an alternative therapy in the 1970s. Nonetheless, continuing research is investigating safer methods of activating Laetrile for targeted cancer treatment. This opens interesting prospects in using these compounds in alternative medical therapies, for which, however, further research is needed.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 3","pages":"205-220"},"PeriodicalIF":3.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051756","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":"Mammary Gland Reactive Stroma Characterization at Aging After Bisphenol A Exposure During Hormonal Susceptibility Windows","authors":"Gervásio Evangelista Brito Filho,&nbsp;Thalles Fernando Rocha Ruiz,&nbsp;Lorena Gabriela de Souza,&nbsp;Luara Jesus Ferrato,&nbsp;Fernanda Cristina Alcantara dos Santos,&nbsp;Patricia Simone Leite Vilamaior,&nbsp;Ellen Cristina Rivas Leonel,&nbsp;Sebastião Roberto Taboga","doi":"10.1002/cbin.12280","DOIUrl":"10.1002/cbin.12280","url":null,"abstract":"<div>\u0000 \u0000 <p>Mammary glands development is influenced by endocrine signaling, which remodels epithelial and stromal compartments. Reactive stroma phenotype is observed when stromal disturbances occur, leading to changes in extracellular matrix composition and occurrence of reactive cell types. One of the triggers of these alterations is endocrine-disrupting chemical exposure, such as bisphenol A (BPA). Studies suggest that BPA acts on receptor binding sites of several hormones interfering the endocrine response. The aim of this study was to investigate the reactive stroma features on mammary glands of aged female gerbils (<i>Meriones unguiculatus</i>) exposed to BPA during windows of susceptibility. Thus, the analysis of cellular profile and growth factor expressions was provided. Fibroblastic population changed in BPA-exposed mammary glands, with a remarkable increase of myofibroblasts (vimentin⁺/α-SMA⁺) and active fibroblasts (FAP⁺). Normal fibroblasts (vimentin⁺/α-SMA⁻) were decreased mainly associated with the increase of FGF-10, an inductor of fibroblastic polarization. CD34⁺ stromal cells were also identified and detected among epithelial cells after BPA-induction disruption. Angiogenesis was supported by VEGF increasing in the gland tissue, which promoted an increase in blood vessel density. Thus, our results demonstrated that reactive stroma was raised in the mammary gland after BPA exposure. This profile was supported by changes in the fibroblastic population due to an induction to synthetic phenotypes and the expression of FGF-10, as well as the angiogenic activity that could corroborate with the malignancy and aggressiveness induced by BPA exposure.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"397-406"},"PeriodicalIF":3.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051758","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":"Delving Into lncRNA-Mediated Regulation of Autophagy-Associated Signaling Pathways in the Context of Breast Cancer","authors":"Chou-Yi Hsu,&nbsp;Saade Abdalkareem Jasim,&nbsp;Pooja Bansal,&nbsp;Harpreet Kaur,&nbsp;Irfan Ahmad,&nbsp;Abdulnaser Saud,&nbsp;Mahamedha Deorari,&nbsp;Zuhair I. Al-Mashhadani,&nbsp;Abhinav Kumar,&nbsp;Ahmed Hussein Zwamel","doi":"10.1002/cbin.12277","DOIUrl":"10.1002/cbin.12277","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer is a multifaceted and prevalent malignancy, impacting a considerable proportion of women globally. Numerous signaling pathways intricately regulate cellular functions such as growth, proliferation, and survival. Among the various regulators, lncRNAs have emerged as significant players despite their inability to encode proteins. An expanding body of literature underscores the pivotal roles lncRNAs play in cancer biology, particularly in the context of breast cancer. Autophagy, the cellular process dedicated to the degradation and recycling of cellular components, is now recognized as a crucial factor in cancer initiation and progression. The interplay between lncRNAs, various signaling pathways, and autophagy in the pathophysiology of breast cancer remains an active area of investigation. Researchers have identified specific lncRNAs that are dysregulated in breast cancer patients, influencing the modulation of key signaling pathways. Using experimental methodologies and bioinformatics approaches, multiple lncRNAs have been elucidated, providing deeper insights into their contributions to breast cancer pathogenesis and metastatic processes. In summary, the pathophysiological landscape of breast cancer is characterized by the complex interactions involving lncRNA-mediated autophagy. This understanding paves the way for identifying novel therapeutic targets, prognostic markers, and diagnostic markers, ultimately contributing to improved treatment outcomes in breast cancer management.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 3","pages":"221-234"},"PeriodicalIF":3.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051757","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":"Hypoxic Cancer Cells-Derived Exosomes Strengthen the Development of Cancer Stem Cell-Like Properties Through Delivering LINC00665 in Thyroid Cancer Cells","authors":"Ming Zhou,&nbsp;Chengcheng Peng,&nbsp;Qiong Zhang,&nbsp;Yanchu Tong","doi":"10.1002/cbin.12274","DOIUrl":"10.1002/cbin.12274","url":null,"abstract":"<div>\u0000 \u0000 <p>Hypoxia is a common phenomenon for solid tumors due to a lack of effective vascular system, and has been deemed as an important factor that drives the progression of thyroid cancer (TC) via altering the characteristics of tumor cells. The present study suggested that hypoxic TC cells enhanced cancer stem cell properties and progression of TC by delivering long intergenic non-protein coding RNA 665 (LINC00665)-containing exosomes. Specifically, TPC1 cells were exposed to normoxic or hypoxic environment, and it was found that hypoxic TPC1 cells-secreted exosomes (H-exo) were enriched with LINC00665, compared to normoxic TPC1 cells-derived exosomes (N-exo). In addition, by establishing the in vitro exosomes-TC cells coculture system, we found that in contrast to N-exo, H-exo apparently promoted cell proliferation, epithelial mesenchymal transition (EMT) and cancer stem cell properties via delivering LINC00665. This was supported by the in vivo results that H-exo transferred LINC00665 to promote tumorigenesis and the expression of EMT and stemness-associated markers in xenograft tumor-bearing mice models. Further mechanical experiments validated that LINC00665 combined with EPHB4 mRNA to sustain its stability to enhance cancer aggressiveness of TC. Altogether, our findings verified that hypoxic TC cells-secreted exosomes regulated the LINC00665/EPHB4 axis to enhance cancer stem cell properties of TC, providing novel signatures for TC diagnosis and therapy.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"384-396"},"PeriodicalIF":3.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000817","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":"Leishmania (Leishmania) amazonensis and Leishmania (Leishmania) infantum sialic acids enhance macrophage infection","authors":"Tainá Cavalcante,&nbsp;Antônio Moreira Marques,&nbsp;Mariana Medina Medeiros,&nbsp;Tania Carolina Reis,&nbsp;Daniel Quina,&nbsp;Bruna Cunha de Alencar,&nbsp;Giuseppe Palmisano,&nbsp;Beatriz Simonsen Stolf","doi":"10.1002/cbin.12269","DOIUrl":"https://doi.org/10.1002/cbin.12269","url":null,"abstract":"<p>Leishmaniases affect millions of people around the world, caused by <i>Leishmania</i> parasites. <i>Leishmania</i> are transmitted by female sandflies from Phlebotominae subfamily during their blood meals. In mammals, promastigotes are phagocytosed mainly by macrophages, differentiate into amastigotes and multiply. For entry and survival in macrophages, <i>Leishmania</i> uses virulence factors such as surface glycoconjugates. Sialic acids (Sias) are found in terminal portions of glycoconjugates and play important roles in human pathogens. The importance of Sias was explored only in <i>L. (L.) donovani</i>, associated with visceral leishmaniasis in Africa, Asia and Europe. Thus, the aim of this study was to characterize Sias of <i>Leishmania (L.) amazonensis</i> and <i>Leishmania (L.) infantum</i>, related to cutaneous and visceral leishmaniasis in South America, respectively. For that, we analyzed by HPLC-FLD the Sias of promastigotes of <i>L. (L.) amazonensis</i> LV79 and two <i>L. (L.) infantum</i> strains, and of <i>L. (L.) amazonensis</i> axenic amastigotes and amastigotes from paw lesions of infected mice. To evaluate Sias importance in promastigotes, we treated stationary phase parasites with sialidase and infected murine and human macrophages. We detected <i>N</i>-Acetylneuraminic Acid in promastigotes of all strains, with greater abundance in <i>L. (L.) infantum</i>. We identified <i>N</i>-Acetylneuraminic Acid and <i>N</i>-Glycolylneuraminic acid in amastigotes recovered from paw lesion, but only <i>N</i>-Acetylneuraminic Acid in axenic amastigotes. Promastigotes treated with sialidase infected less macrophages than parasites displaying total Sias. Our results demonstrate that Sias vary between <i>Leishmania</i> species and between <i>L. (L.) amazonensis</i> life stages and plays an important role in macrophage infection by <i>L. (L.) amazonensis</i> and <i>L. (L.) infantum</i>.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"357-364"},"PeriodicalIF":3.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571354","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":"Circadian clock gene BMAL1 is involved in transforming growth factor β1-induced fibrotic response in NRK-49F cells","authors":"Akira Takaguri,&nbsp;Ryuta Noro,&nbsp;Sari Shinohe,&nbsp;Reina Murayama,&nbsp;Mei Sakuraba,&nbsp;Reo Nomura,&nbsp;Kumi Satoh","doi":"10.1002/cbin.12273","DOIUrl":"10.1002/cbin.12273","url":null,"abstract":"<p>The transcription factor brain and muscle Arnt-like protein-1 (BMAL1) is a clock protein involved in various diseases, including atherosclerosis and cancer. However, BMAL1's involvement in kidney fibrosis and the underlying mechanisms remain largely unknown, a gap addressed in this study. Analysis through Masson's trichrome and Sirius red staining revealed that all groups exposed to unilateral ureteral obstruction showed increased BMAL1 protein expression accompanied by increased TGF-β1 expression and elevated key fibrosis markers, including α-SMA, compared with sham groups. Although TGF-β1 induced BMAL1 protein expression accompanied by increased α-SMA expression in NRK-49F cells, the REV-ERBα agonist GSK4112, a transcriptional repressor of BMAL1, or siRNA targeting BMAL1 significantly inhibited TGF-β1-induced α-SMA expression. Furthermore, BMAL1 knockdown significantly suppressed TGF-β1-induced NOX4/ROS/p38 pathways in NRK-49F cells. Thus, BMAL1 positively regulates TGF-β1-induced signaling associated with fibrotic responses via the NOX4/ROS/p38 pathway. Overall, this study uncovers BMAL1 as a promising therapeutic target for preventing and treating kidney fibrosis, potentially preventing renal failure.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"365-373"},"PeriodicalIF":3.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930801","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}