BioFactors最新文献

{"title":"Correction to “Pathophysiology of Endoplasmic Reticulum Stress and the Potential Role of Dexmedetomidine as a Modulator”","authors":"","doi":"10.1002/biof.70046","DOIUrl":"10.1002/biof.70046","url":null,"abstract":"<p>N. Karamali, R. K. Moghadam, M. B. Farahan, et al., “Pathophysiology of Endoplasmic Reticulum Stress and the Potential Role of Dexmedetomidine as a Modulator,” <i>BioFactors</i> 51, no. 4 (2025): e70022, https://doi.org/10.1002/biof.70022.</p><p>In this originally-published article, author Negin Karamali's affiliation was incorrect. The correct version is shown below. This has been updated in the online version of this article.</p><p>Incorrect</p><p>¹Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran</p><p>Correct</p><p>¹Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran</p><p>We apologize for this error.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://iubmb.onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111247","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":"The Role of STAT3 in Cancer: From Metabolic Regulation to Therapeutic Targeting","authors":"Maryam Ashourpour,&nbsp;Jamal Mohammadian,&nbsp;Amir Mehdizadeh,&nbsp;Mina Afrashteh Nour,&nbsp;Amir Ghorbanihaghjo","doi":"10.1002/biof.70045","DOIUrl":"10.1002/biof.70045","url":null,"abstract":"<div>\u0000 \u0000 <p>Cancer is one of the major public health challenges worldwide, and the STAT3 signaling pathway is recognized as one of the most important signaling pathways in the progression of this disease. This pathway can increase the survival and proliferation of cancer cells and their resistance to treatment by regulating lipid and carbohydrate metabolism, apoptosis, and inflammatory processes. Therefore, STAT3 inhibition is considered an effective therapeutic approach in the fight against cancer. Two main strategies (direct and indirect) have been considered to inhibit this protein, with direct inhibition being more effective due to its more specific properties. Extensive research is also underway to design and develop effective inhibitors for STAT3, and in this regard, SH2 domain inhibitors have reached clinical trial phases.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145012431","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 Therapeutic Potential of Flavonols in Alzheimer's Disease: Inhibiting Amyloid-β, Oxidative Stress, and Neuroinflammation","authors":"Mohammad Yasin Zamanian,&nbsp;Lusine G. Khachatryan,&nbsp;Mahzad Heidari,&nbsp;Razieh Darabi,&nbsp;Maryam Golmohammadi,&nbsp;Raed Fanoukh Aboqader Al-Aouadi,&nbsp;Esra Küpeli Akkol","doi":"10.1002/biof.70047","DOIUrl":"10.1002/biof.70047","url":null,"abstract":"<div>\u0000 \u0000 <p>Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) aggregation, oxidative stress, and neuroinflammation, remains a significant global health challenge. This study investigates the therapeutic potential of flavonols—quercetin, kaempferol, myricetin, and fisetin—in targeting Aβ aggregation and mitigating AD pathology through diverse molecular mechanisms. Our findings reveal that flavonols effectively inhibit Aβ oligomerization and fibril formation, reduce oxidative stress via Nrf2/HO-1 pathway activation, and suppress neuroinflammation by modulating microglial polarization. Additionally, these compounds enhance mitochondrial function, promote autophagy-mediated clearance of Aβ aggregates, and regulate key enzymes such as β-secretase (BACE1) and α-secretases (ADAM10/17), favoring non-amyloidogenic pathways. Quercetin demonstrated neuroprotective effects by activating TrkB signaling, reducing tau phosphorylation, and enhancing synaptic plasticity. Kaempferol prevented Aβ-induced apoptosis via the ER/ERK/MAPK pathway and inhibited acetylcholinesterase activity, improving cognitive outcomes. Myricetin ameliorated mitochondrial dysfunction and oxidative damage through GSK3β/ERK2 signaling modulation and showed enhanced brain bioavailability when delivered via nanostructured lipid carriers. Fisetin reduced Aβ burden by upregulating neprilysin expression, suppressed neuroinflammation, and improved synaptic function by restoring synaptic protein levels. Overall, flavonols exhibit multi-targeted therapeutic potential against AD by addressing its complex pathogenesis. Their ability to cross the blood–brain barrier and low toxicity profiles position them as promising candidates for further clinical development. This study underscores the potential of flavonols as natural agents for AD treatment and highlights their role in advancing multi-mechanistic therapeutic strategies.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144930099","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":"Knocking Down SKA1 Inhibits Hepatocellular Carcinoma Progression via Apoptosis: Integrating Single-Cell Transcriptomics With In Vivo and In Vitro Validation","authors":"Qiong Luo,&nbsp;Qianyuan Zhang,&nbsp;Ziying Zheng,&nbsp;Xiaoyan Jiang","doi":"10.1002/biof.70044","DOIUrl":"10.1002/biof.70044","url":null,"abstract":"<div>\u0000 \u0000 <p>Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer. Spindle- and kinetochore-associated complex 1 (SKA1) participates in the regulation of mitosis, playing an essential role in regulating cancer progression. Therefore, this study aims to explore the effects of knocking down SKA1 on HCC. The bioinformatics analysis approaches were adopted to predict SKA1 expression in HCC, the role of SKA1 on the survival rate and prognosis of HCC patients, and the associations between SKA1 expression and gene mutation and immune cell infiltration. The single-cell transcriptome sequencing analysis was employed to explore the cell–cell communications and molecular interactions. The CCK-8, wound healing, Transwell, flow cytometry, and qRT-PCR approaches were used to determine the cell viability, invasion, migration, cell cycle, apoptosis, and SKA1 mRNA expression level of SMMC7721 cells. The tumor volume and weight were measured. The Western blot was applied to determine the protein expression levels of SKA1, survivin, Bax, Bad, Bcl-2, caspase-3, and caspase-9 in SMMC7721 cells and tumor tissue. The bioinformatics analysis results indicated that highly expressed SKA1 was related to a low survival rate and poor prognosis of HCC patients and was involved in the TP53 mutation and multiple immune cell infiltrations. The single-cell transcriptome sequencing analysis affirmed that malignant cells were associated with hepatocytes, ILC, and granulocytes. Meanwhile, various pathways and ligand-receptor pairs were enriched in the cell subpopulation with high SKA1 expression, especially for the Protease-Activated Receptors (PARs) pathway and MDK-SDC1 pair associated with the apoptosis signaling. Knocking down SKA1 reduced the cell viability, invasion, and migration, arrested the cell cycle in the S period, promoted the apoptosis in vitro, decreased the tumor volume and weight in vivo, and down-regulated the survivin and Bcl-2 protein expression levels and up-regulated the caspase 3, caspase 9, Bax, and Bad in vivo and in vitro. Taken together, knocking down SKA1 inhibited HCC progression by promoting the apoptosis signaling pathway.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910393","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":"Formation of Plant Derived Bioactive Peptides During Simulated Gastro-Intestinal Digestion: A Systematic Review","authors":"Stefania Iametti,&nbsp;Alessandra Bordoni,&nbsp;Mattia Di Nunzio","doi":"10.1002/biof.70043","DOIUrl":"10.1002/biof.70043","url":null,"abstract":"<div>\u0000 \u0000 <p>A plant-based diet is known to be nutrient-dense and rich in fibers, healthy fats, proteins, vitamins, and minerals. A diet rich in plant-based foods may help reduce the risk of chronic diseases such as cardiovascular disease and diabetes. As consumers become more health conscious, there is a growing interest in plant-based diets. In addition to providing essential nutrients, some food proteins may provide additional health benefits, as plant proteins are broken down into bioactive peptides during gastrointestinal digestion, often in dependence on previous processing. Bioactive peptides have several important functions in the body, including antioxidant, antimicrobial, immunomodulatory, and anti-hypertensive effects. To date, several reviews have provided an overview of the generation of bioactive peptides and their associated biological activities and putative health benefits in a range of animal-based foods, but information on plant-based foods is fragmented. We then systematically reviewed the existing literature reporting the release of bioactive peptides from plant-based food products and ingredients after in vitro digestion according to the INFOGEST protocol. The results reported in this review highlight that most of the bioactive peptides of plant origin exhibited antioxidant, anti-hypertensive, and anti-diabetic activity. The relationship between the structure and functionality of peptides and the major gaps in bioactive peptide research were also discussed, to focus on these aspects in future research. This may lead to a better understanding of the behavior of plant proteins in the human gastrointestinal tract, enhancing their contribution as sources of bioactive peptides.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881386","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":"Correction to “Proteins and Carbon Dioxide Struggle Against Peroxynitrite”","authors":"","doi":"10.1002/biof.70040","DOIUrl":"10.1002/biof.70040","url":null,"abstract":"&lt;p&gt;G. De Simone, A. di Masi, G. R. Tundo, et al., “Proteins and Carbon Dioxide Struggle Against Peroxynitrite,” &lt;i&gt;BioFactors&lt;/i&gt; 51, no. 4 (2025): e70030, 10.1002/biof.70030.&lt;/p&gt;&lt;p&gt;In the originally published article, the title of Table 2 is incorrect. The correct title is shown below.&lt;/p&gt;&lt;p&gt;Incorrect&lt;/p&gt;&lt;p&gt;Values of &lt;span&gt;&lt;/span&gt;&lt;math&gt;\u0000 &lt;semantics&gt;\u0000 &lt;mrow&gt;\u0000 &lt;msubsup&gt;\u0000 &lt;mi&gt;k&lt;/mi&gt;\u0000 &lt;mn&gt;0&lt;/mn&gt;\u0000 &lt;mi&gt;obs&lt;/mi&gt;\u0000 &lt;/msubsup&gt;\u0000 &lt;/mrow&gt;\u0000 &lt;annotation&gt;$$ {k}_0^{obs} $$&lt;/annotation&gt;\u0000 &lt;/semantics&gt;&lt;/math&gt; for various actors of peroxynitrite decomposition, predicted on the basis of their physiological concentration reported in Table 1.&lt;/p&gt;&lt;p&gt;Correct&lt;/p&gt;&lt;p&gt;Values of &lt;span&gt;&lt;/span&gt;&lt;math&gt;\u0000 &lt;semantics&gt;\u0000 &lt;mrow&gt;\u0000 &lt;msubsup&gt;\u0000 &lt;mi&gt;k&lt;/mi&gt;\u0000 &lt;mn&gt;0&lt;/mn&gt;\u0000 &lt;mi&gt;obs&lt;/mi&gt;\u0000 &lt;/msubsup&gt;\u0000 &lt;/mrow&gt;\u0000 &lt;annotation&gt;$$ {k}_0^{obs} $$&lt;/annotation&gt;\u0000 &lt;/semantics&gt;&lt;/math&gt; for various actors of peroxynitrite decomposition were predicted on the basis of data reported in Table 1.&lt;/p&gt;&lt;p&gt;Incorrect&lt;/p&gt;&lt;p&gt;4.1 The Thiol-Protein-Dependent Inactivation of Peroxyinitrite.&lt;/p&gt;&lt;p&gt;Correct&lt;/p&gt;&lt;p&gt;4.1 The Thiol-Protein-Dependent Inactivation of Peroxynitrite.&lt;/p&gt;&lt;p&gt;On the second line of Table 2, CO&lt;sub&gt;2&lt;/sub&gt; (extracellular)&lt;sup&gt;b&lt;/sup&gt; is incorrectly spelled as CO&lt;sub&gt;2&lt;/sub&gt; (extracellare).&lt;sup&gt;b&lt;/sup&gt;&lt;/p&gt;&lt;p&gt;In Section 5, the following text is incorrect. The correct text is shown below.&lt;/p&gt;&lt;p&gt;Incorrect&lt;/p&gt;&lt;p&gt;As a matter of fact, since the average Hb concentration in the blood is 8.0 × 10&lt;sup&gt;−3&lt;/sup&gt; M (resulting from the intraerythrocytic concentration 2.0 × 10&lt;sup&gt;−2&lt;/sup&gt; M times the hematocrit of 40%) and the value of (= 8.8 × 10&lt;sup&gt;4&lt;/sup&gt; M&lt;sup&gt;−1&lt;/sup&gt; s&lt;sup&gt;−1&lt;/sup&gt;; Table 1), the expected maximal rate for peroxynitrite isomerization = 700 s&lt;sup&gt;−1&lt;/sup&gt;; therefore, HbO&lt;sub&gt;2&lt;/sub&gt; indeed is potentially more efficient than carbon dioxide in the reaction from peroxynitrite, this being especially relevant as a boost during the rising of peroxynitrite after the deactivation of PRDXs. However, the reaction of HbO&lt;sub&gt;2&lt;/sub&gt; brings about the oxidation of a portion of it (never exceeding 10% of whole HbO&lt;sub&gt;2&lt;/sub&gt;), even though Hb(III) participates to peroxynitrite scavenging as well; therefore, after the initial powerful boost from HbO&lt;sub&gt;2&lt;/sub&gt; a steady-state role of peroxynitrite isomerization, corresponding to the average 10% of Hb(III) (i.e., ≈ 8.0 × 10&lt;sup&gt;−4&lt;/sup&gt; M) [75], suggests a constant rate ≈ 30 s&lt;sup&gt;−1&lt;/sup&gt; (corresponding to = 3.9 × 10&lt;sup&gt;4&lt;/sup&gt; M&lt;sup&gt;−1&lt;/sup&gt; s&lt;sup&gt;−1&lt;/sup&gt; for Hb(III); Table 1).&lt;/p&gt;&lt;p&gt;Correct&lt;/p&gt;&lt;p&gt;As a matter of fact, since the average Hb concentration in the blood is 8.0 × 10&lt;sup&gt;−3&lt;/sup&gt; M and","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://iubmb.onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144832875","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":"Diverse Inhibitors of De Novo Purine Synthesis Promote AICAR-Induced AMPK Activation and Glucose Uptake in L6 Myotubes","authors":"Klemen Dolinar,&nbsp;Katarina Miš,&nbsp;Katja Šopar,&nbsp;Mateja Šutar,&nbsp;Meta Božič,&nbsp;Matic Kolar,&nbsp;Tim Hropot,&nbsp;Pablo M. Garcia-Roves,&nbsp;Alexander V. Chibalin,&nbsp;Sergej Pirkmajer","doi":"10.1002/biof.70037","DOIUrl":"10.1002/biof.70037","url":null,"abstract":"<p>Methotrexate, an immunosuppressant and anticancer drug, promotes glucose uptake and lipid oxidation in skeletal muscle via activation of AMP-activated protein kinase (AMPK). Methotrexate promotes AMPK activation by inhibiting 5-aminoimidazole-4-carboxamide ribonucleotide (ZMP) formyltransferase/inosine monophosphate (IMP) cyclohydrolase (ATIC), which converts ZMP, an endogenous purine precursor and an active form of the pharmacological AMPK activator AICAR, to IMP during de novo purine synthesis. In addition to methotrexate, inhibition of purine synthesis underpins the therapeutic effects of a number of commonly used immunosuppressive, anticancer, and antimicrobial drugs, raising the question of whether activation of AMPK in skeletal muscle could be a recurrent feature of these drugs. Using L6 myotubes, we found that AICAR-induced AMPK activation and glucose uptake were enhanced by inhibitors of the conversion of IMP to GMP (mycophenolate mofetil) or of IMP to AMP (alanosine) as well as by indirect inhibitors of human (trimetrexate) and bacterial ATIC (sulfamethoxazole). 6-Mercaptopurine, which inhibits the conversion of IMP to GMP and AMP, activated AMPK, increased glucose uptake, and suppressed insulin signaling, but did not enhance the effect of AICAR. As determined by measuring oxygen consumption rate, none of these agents suppressed mitochondrial function. Overall, our results indicate that IMP metabolism is a gateway for the modulation of AMPK and its metabolic effects in skeletal muscle cells.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://iubmb.onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144814822","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":"Pathophysiology of Endoplasmic Reticulum Stress and the Potential Role of Dexmedetomidine as a Modulator","authors":"Negin Karamali,&nbsp;Reihaneh Khaleghi Moghadam,&nbsp;Mohammad Borzabadi Farahani,&nbsp;Arman Rostamlou,&nbsp;Mirhamed Hoseini-Aghdam,&nbsp;Amirhossein Mardi,&nbsp;Behzad Baradaran,&nbsp;Leili Aghebati-Maleki","doi":"10.1002/biof.70022","DOIUrl":"10.1002/biof.70022","url":null,"abstract":"<div>\u0000 \u0000 <p>Endoplasmic reticulum (ER) stress is a fundamental process that profoundly influences immune cell function and plays a critical role in the development and progression of various physiological and pathological conditions. Understanding the underlying mechanisms of ER stress and its implications for cellular function and disease pathogenesis is of paramount importance in developing targeted therapeutic interventions. Dexmedetomidine, an alpha-2 adrenergic agonist primarily used as a sedative, has emerged as a potential modulator of ER stress. This review aims to explore the impact of Dexmedetomidine on ER stress within immune cells and its potential therapeutic implications. Dexmedetomidine exhibits the remarkable ability to inhibit the activation of ER stress pathways, preserve protein synthesis, and suppress apoptosis mediated by ER stress markers. Furthermore, Dexmedetomidine exerts regulatory effects on immune cells and inflammation by reducing the production of proinflammatory cytokines and modulating immune functions. These compelling findings suggest that Dexmedetomidine holds significant promise as a valuable therapeutic tool for conditions characterized by dysregulated ER stress and immune dysfunction.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144809224","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":"Profiling of RUVBL2-Induced Transcriptome Alterations Highlights a Critical Role for Chromatin Remodeling in Ovarian Cancer","authors":"Renhao Xue,&nbsp;Yingjie Wang,&nbsp;Xiaomei Luo,&nbsp;Hao Zhang,&nbsp;Dongcheng Guan,&nbsp;Shuo Shi,&nbsp;Yu Wang","doi":"10.1002/biof.70041","DOIUrl":"10.1002/biof.70041","url":null,"abstract":"<div>\u0000 \u0000 <p>Cancerous transcriptome alterations in carcinoma cells could be originated from either genetic copy number changes or epigenetic reprogramming. Ovarian cancer (OV) is the most malignant gynecologic tumor, known for high aneuploidy with robust copy number alterations. However, low aneuploidy ovarian tumors are also frequently found, indicating an essential contribution of epigenetic factors during tumorigenesis and cancer development. Chromatin remodeling modulates the transcriptome epigenetically in a variety of cancer types, but its role in OV is still unclear. Hence, we investigated a cohort of 102 OV patients, analyzed transcriptomic and clinical data from public databases, and performed cellular experiments. We found that RUVBL2, a subunit of the INO80 complex, functions as the key oncogenic chromatin remodeler in OV. RUVBL2 is upregulated in tumors, particularly in low-aneuploidy cases, and is associated with poor prognosis. RUVBL2 drives nucleosome dynamics and elevates chromatin accessibility selectively at promoter regions. The landscape of RUVBL2-dependent modulation of chromatin accessibility and the transcriptome exhibits activation of various transcription factors, especially the AP-1 family, and upregulation of a series of key genes, including <i>CDKN3</i>, <i>MYBL2</i>, and <i>ZNF144</i>, resulting in mediation of cell cycle and Hippo signaling pathway to promote DNA synthesis and cell proliferation. Hence, RUVBL2-dependent chromatin remodeling plays a key role in oncogenic reprogramming of the transcriptome in OV. These findings provide novel insights into the molecular etiology of OV and disclose potential biomarkers and drug targets.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767554","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":"Curcumin Induces Transgenerational and Sex-Specific Effects on Lifespan, Gene Expression, and Metabolism in the Fruit Fly Drosophila melanogaster","authors":"Silvana Hof-Michel,&nbsp;Belén Olga Ferrando Hernandez,&nbsp;Andreas Vilcinskas,&nbsp;Anika E. Wagner","doi":"10.1002/biof.70039","DOIUrl":"10.1002/biof.70039","url":null,"abstract":"<p>Curcumin is a bioactive compound found in turmeric (<i>Curcuma longa</i>) and is widely recognized for its health-promoting effects, including anti-inflammatory, antioxidant, and anti-carcinogenic properties. It can also mediate epigenetic effects by inhibiting histone acetylases (HATs) and deacetylases (HDACs) but the transgenerational context has not been studied in detail. Here, we used the fruit fly (<i>Drosophila melanogaster</i>) as a model organism to determine the epigenetic effects of 0.1% and 1% (w/v) curcumin, which have been shown to promote the health and prolong the lifespan of fruit flies. Both concentrations were found to significantly increase lifespan and climbing activity in male and female flies, but changes in HAT/HDAC gene expression and metabolism were sex-specific. Unexpectedly, the F1 offspring of curcumin-treated parental flies showed a significant reduction in lifespan that was also sex-specific, as well as sex-specific and dose-dependent transgenerational changes in HAT/HDAC gene expression and metabolism. These results show that curcumin's beneficial effects in the parental generation are followed by deleterious effects in the offspring, highlighting the need to further investigate the potential transgenerational effects of nutrients and bioactive compounds that are used as dietary supplements for humans.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758546","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}