Molecular and Cellular Biochemistry最新文献

{"title":"Risk factors for mild cognitive impairment in Parkinson disease: a systematic review and meta-analysis.","authors":"Yaodan Zhang, Fang Chen, Fengchun Ren","doi":"10.1007/s11010-025-05392-y","DOIUrl":"https://doi.org/10.1007/s11010-025-05392-y","url":null,"abstract":"<p><strong>Background: </strong>Mild cognitive impairment (MCI) is a common non-motor manifestation of Parkinson's disease (PD) and often precedes dementia. However, evidence on its demographic and clinical risk factors remains inconsistent. This study aimed to synthesize available data through a meta-analysis to identify determinants of MCI in PD.</p><p><strong>Methodology: </strong>This systematic review and meta-analysis followed PRISMA guidelines. Electronic databases were searched using MeSH terms and validated keywords. Studies were selected through a multi-step screening process by independent reviewers. Data extraction and quality assessment were performed using the Newcastle-Ottawa Scale. Meta-analyses were conducted using Comprehensive Meta-Analysis (v2). Random- or fixed-effects models were applied based on heterogeneity (I² threshold = 50%). Beggs and Mazumdar test assessed publication bias, with significance set at (P < 0.1).</p><p><strong>Results: </strong>This meta-analysis included 33 studies, Significant risk factors for MCI in individuals with PD included older age (effect size = 0.4, 95% CI: 0.315-0.498, P ≤ 0.001), older age at disease onset (effect size = 0.18, 95% CI: 0.05-0.327, P ≤ 0.001), and longer disease duration (effect size = 0.14, 95% CI: 0.08-0.2, P ≤ 0.001). Higher educational attainment showed a protective effect (effect size = -0.438, 95% CI: -0.555 to -0.321, P ≤ 0.001). No significant association was found between gender and MCI (OR = 0.899, 95% CI: 0.749-1.079, P = 0.253). Disease severity, based on UPDRS and Hoehn and Yahr scales, was significantly associated with increased MCI risk.</p><p><strong>Conclusion: </strong>Advanced age, later disease onset, longer disease duration, and greater severity are key risk factors for MCI in PD. These findings highlight the need for early detection and proactive management to guide clinical decisions.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.","authors":"Ana Grego, Cristiana Fernandes, Ivo Fonseca, Marina Dias-Neto, Raquel Costa, Adelino Leite-Moreira, Sandra Marisa Oliveira, Fábio Trindade, Rita Nogueira-Ferreira","doi":"10.1007/s11010-025-05390-0","DOIUrl":"https://doi.org/10.1007/s11010-025-05390-0","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: HIV-1 genome-encoded hiv1-mir-H1 impairs cellular responses to infection.","authors":"Deepak Kaul, A Ahlawat, Sunny Duttagupta","doi":"10.1007/s11010-025-05383-z","DOIUrl":"https://doi.org/10.1007/s11010-025-05383-z","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145070066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The many ways to inhibit translation by Sorafenib in liver cancer cells.","authors":"Laura Contreras, Sara Ricciardi, Stefano Biffo, Jordi Muntané, Jesús de la Cruz","doi":"10.1007/s11010-025-05391-z","DOIUrl":"https://doi.org/10.1007/s11010-025-05391-z","url":null,"abstract":"<p><p>Sorafenib targets various tyrosine kinase receptors, inhibiting cell growth and proliferation, angiogenesis and metastasis in tumour cells. It is used to treat certain types of cancers including renal, thyroid and liver (hepatocellular carcinoma) cancers. Although Sorafenib is approved for advanced hepatocellular carcinoma, it only extends patient´s lives by a few months, highlighting the urgent need to better understand how it works and to develop more effective treatments. Sorafenib specifically inhibits translation initiation in hepatocellular carcinoma cells. Herein, we revealed that this inhibition results, at least, from the activation of PERK, triggering a stress response that leads to eIF2α phosphorylation, the inhibition of MNK1a-signalling-dependent eIF4E phosphorylation, and the aberrant assembly of the canonical eIF4F complex. Sorafenib also inhibits the ERK1/2 MAPK signalling in HepG2 cells. However, the mTORC1 pathway does appear to play a pivotal role in Sorafenib-dependent translation inhibition, as revealed by the phosphorylation levels of RPS6 and 4EBP1 proteins and the effects on translation of gene silencing 4EBP1/2 in Sorafenib-treated cells. Translation inhibition correlates with reduced production of cancer-promoting proteins like Cyclin D1 and c-Myc. Overexpression of the phosphomimetic eIF4E-S209D variant, which constitutively activates eIF4E, shows that inhibition of eIF4E phosphorylation directly causes Cyclin D1 down-regulation and cell-cycle delay in Sorafenib-treated cells. Taken together, our results confirm that Sorafenib induces translation reprogramming, whose understanding is crucial for improving its efficacy as a cancer therapy.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145065064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Balancing senescence and apoptosis: therapeutic insights into aging and cancer.","authors":"Nusrat Jan, Shazia Sofi, Aijaz Ahmad Mir, Gowhar Masoodi, Manzoor Ahmad Mir","doi":"10.1007/s11010-025-05388-8","DOIUrl":"10.1007/s11010-025-05388-8","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The oncogenic role of NSUN2 in lung adenocarcinoma by stabilizing CCT5 mRNA via a YBX1-dependent m5C modification.","authors":"Minxia Li, Ning Du, Ping Tang","doi":"10.1007/s11010-025-05378-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05378-w","url":null,"abstract":"<p><p>5-methylcytosine (m5C) methylation is a post-transcriptional modification of RNAs, and its dysregulation plays pro-tumorigenic roles in lung adenocarcinoma (LUAD). Here, this study elucidated the mechanism of action of NSUN2, a major m5C methyltransferase, on LUAD progression. mRNA expression was analyzed by quantitative PCR. Protein expression was tested by immunohistochemistry and immunoblotting. Cell proliferation was evaluated by MTT and EdU assays. Cell apoptosis was detected by flow cytometry and TUNEL staining. Transwell assays were used to examine cell invasion and migration. The influence of NSUN2 or the m5C reader YBX1 in CCT5 mRNA was analyzed by RNA immunoprecipitation assay and Actinomycin D treatment. In human LUAD, NSUN2 expression was upregulated, and high NSUN2 expression foreboded worse overall survival of LUAD patients. NSUN2 knockdown suppressed cell proliferation, diminished invasive and migratory potentials, and stimulated apoptosis in LUAD cells. NSUN2 was positively associated with CCT5 expression in LUAD and could mediate m5C modification of CCT5 mRNA. NSUN2 enhanced CCT5 mRNA stability and protein expression via two specific cysteines (C271 and C321). Moreover, YBX1 promoted CCT5 mRNA stability and protein expression. Additionally, restoration of CCT5 expression abolished NSUN2 deletion-mediated in vitro anti-proliferation, pro-apoptosis, anti-migration, and anti-invasiveness effects in LUAD cells, as well as in vivo anti-tumor growth behavior. Our study indicates that NSUN2 enhances the stability of CCT5 mRNA through a YBX1-m5C-dependent manner to drive LUAD progression. Targeting the NSUN2/CCT5 axis may be a potential approach to combat LUAD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.","authors":"Zhen Xu, Shuo Yang, Yuan Tan, Qian Zhang, He Wang, Jingjin Tao, Qi Liu, Qingchen Wang, Weimin Feng, Zhongxin Li, Chong Wang, Liyan Cui","doi":"10.1007/s11010-025-05379-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05379-9","url":null,"abstract":"<p><p>Cardiovascular-Kidney-Metabolic (CKM) syndrome, a newly defined systemic disorder, is characterized by the pathological interplay among diabetes, chronic kidney disease (CKD), and cardiovascular disease (CVD). Recent studies have identified chronic inflammation not only as a central mediator in the pathological progression of CKM syndrome but also as a pivotal molecular hub that drives coordinated damage across multiple organ systems. Mechanistic investigations have revealed that aberrant activation of signaling pathways such as NF-κB, Wnt, PI3K-AKT, JAK-STAT, and PPAR constitutes a complex inflammatory regulatory network. Notably, these pathways facilitate inter-organ inflammatory crosstalk, establishing positive feedback loops among the heart, kidneys, and metabolic tissues. This, in turn, amplifies pathological processes such as oxidative stress, endothelial dysfunction, and fibrosis in a cascading manner.This review systematically delineates the multidimensional pathophysiological mechanisms of CKM syndrome, with particular emphasis on the inter-organ inflammatory regulation mediated by key signaling pathways. Furthermore, we explore the translational potential of therapeutic strategies targeting inflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α) based on the latest clinical evidence, aiming to provide a theoretical framework and novel perspectives for disrupting the vicious cycle of CKM syndrome.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Spironolactone inhibits apoptosis in rat mesangial cells under hyperglycaemic conditions via the Wnt signalling pathway.","authors":"Dan Zhu, Hongwei Yu, Hongjiang He, Jiuli Ding, Jie Tang, Dan Cao, Lirong Hao","doi":"10.1007/s11010-025-05389-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05389-7","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the beneficial effects of curcumin-based hydrogel beads in rats with rheumatoid arthritis induced by Freund's complete adjuvant.","authors":"Katarina Djordjevic, Bozidar Pindovic, Katarina Mihajlovic, Igor Ilic, Jelena Terzic, Andjela Milojevic-Samanovic, Zorka Stanic, Katarina Postolovic, Natalia Ekkert, Vladimir Reshetnikov, Vladimir Zivkovic, Vladimir Jakovljevic, Tamara Nikolic Turnic","doi":"10.1007/s11010-025-05380-2","DOIUrl":"https://doi.org/10.1007/s11010-025-05380-2","url":null,"abstract":"<p><p>The aim of this study was to examine the potential antioxidant activity of curcumin in therapeutic and preventive condition and its potential role as adjuvant to conventional drug methotrexate in treatment of rheumatoid arthritis (RA). The study included 104 female Wistar albino rats, 6 weeks old, body weight of 200-250 g, which were divided into 8 groups (n=13 in each group): 1. CTRL: negative control, 2. CUR: positive control 1 (curcumin 200 mg/kg three times a week for 4 weeks per os), 3. MTX: positive control 2 (methotrexate 0,75 mg/kg i.p. two times a week for 4 weeks), 4. RA: positive control 3 (induced RA), 5. RA+pCUR: rats with induced RA + preventive administration of curcumin (curcumin 200 mg/kg three times a week for 4 weeks per os before the induction of RA), 6. RA+tCUR: rats with induced RA + curcumin therapy, 7. RA+MTX+pCUR; rats with induced RA + preventive administration of curcumin + methotrexate 0.75 mg/kg i.p. twice weekly for 4 weeks, 8. RA+MTX+tCUR: rats with induced RA + therapeutic administration of curcumin + methotrexate 0.75 mg/kg i.p. twice weekly for 4 weeks. Potential therapeutic effect of curcumin (200 mg/kg three times a week for 4 weeks orally) and RA induction were initiated on the same day; for preventive protocol, curcumin was administered 4 weeks before the start of RA induction at a dose of 200 mg/kg orally three times a week. Rheumatoid arthritis was triggered by administering 0.1 ml of Complete Freund's Adjuvant (CFA) subcutaneously at the base of the rat tail. Rats were sacrificed 28 days after immunization. During the experimental period, we collected data for arthritis score, radiography testing, and blood sample collecting for specific biochemical analysis for prooxidative and antioxidative parameters (superoxide anion radical, hydrogen peroxide, nitric oxide, index of lipid peroxidation, superoxide dismutase, catalase, and reduced glutathione). Our experimental study confirmed that the therapeutic administration of curcumin reduced disease activity and significantly increased the activities of antioxidative enzymes and reduced prooxidants. Also, preventive administration, especially in combination with methotrexate, offers superior protection by limiting the onset and development of oxidative stress. These findings support the claim that curcumin as turmeric can effectively inhibit inflammatory reactions and reduces symptoms through changing the redox status. Future large randomized controlled trials on the effects of turmeric substance are needed.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Keratin 15 promotes tumor growth, invasion, epithelial-mesenchymal transition and radioresistance but represses ferroptosis via a Wnt/β-catenin signaling-related way in breast cancer.","authors":"Jiahui Jin, Peng Zhao, Chengcheng Dai, Jie Li, Ziyi Huang, Tongsong Zhang, Xuezhen Ma","doi":"10.1007/s11010-025-05369-x","DOIUrl":"10.1007/s11010-025-05369-x","url":null,"abstract":"<p><p>Keratin 15 (KRT15) promotes tumor progression in several cancers, but its engagement in breast cancer is seldom uncovered. This study aimed to explore the impact of KRT15 modification on breast cancer growth, mobility, radiosensitivity, ferroptosis, and Wnt/β-catenin signaling pathway. A lentiviral vector containing short hairpin RNA or complementary DNA targeting KRT15 was transfected into MDA-MB-231 and MCF-7 cells in vitro. The transfected MCF-7 cells were further proposed to irradiation treatment. In vivo, female BALB/c nude mice were used to establish xenograft model with KRT15-overexpressed MDA-MB-231 cells and treated by irradiation. KRT15 overexpression promoted cell proliferation, migration, invasion, colony number, epithelial-mesenchymal transition (EMT, reflected by E-Cadherin, N-Cadherin, and Vimentin expressions), and S-stage cell cycle arrest in MDA-MB-231 and MCF-7 cells, but repressed cell apoptosis and ferroptosis (reflected by DMT1, SLC7A11, FTH1, and GPX4 expressions); while KRT15 knockdown exhibited the opposite effects. Importantly, KRT15 overexpression enhanced irradiation resistance in MCF-7 cells reflected by cell proliferation, migration, invasion, colony number, cell cycle, and cell apoptosis detections. Besides, KRT15 overexpression increased EMT and activated Wnt/β-catenin signaling pathway (reflected by β-catenin, TCF-1, c-Myc, CCND1, MMP7 expressions) in MCF-7 cells with or without irradiation. In vivo experiments further validated that KRT15 overexpression promoted tumor growth, EMT, Wnt/β-catenin signaling pathway, and irradiation resistance, but repressed the ferroptosis. Collectively, KRT15 may facilitate tumor growth, invasion, EMT, and radioresistance but represses ferroptosis in a Wnt/β-catenin signaling-related way, suggesting its potency as a treatment target for breast cancer management.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144961524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}