Cytotechnology最新文献

{"title":"Blocking circular RNA FNDC3B induces fibroblast-like synoviocytes dysfunction to ameliorate rheumatoid arthritis through regulating the miR-125a-5p-Hexokinase2 axis.","authors":"Jiaxin Fu, Zhi Liu, Guangxin Zhang, Chun Zhang","doi":"10.1007/s10616-025-00745-3","DOIUrl":"10.1007/s10616-025-00745-3","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic, progressive, autoimmune inflammatory joint disease. The cause of synovitis in rheumatoid arthritis involves the interaction between immune cells/macrophages and fibroblast-like synoviocytes (FLSs-RA). The impact of circular RNAs on FLSs and their role in RA pathology is still unknown. This study aimed to investigate the roles and molecular mechanisms of circular RNA FNDC3B in regulating cell injury and glucose metabolism of FLSs in RA. We demonstrated that circFNDC3B was significantly upregulated and miR-125a-5p was significantly downregulated in FLSs from RA patients. When circFNDC3B was silenced or miR-125a-5p was overexpressed, it reduced FLSs-RA glucose metabolism and increased oxidative stress-induced cell injury. Through bioinformatics analysis, RNA pull-down, and luciferase assays, it was found that circFNDC3B sponged miR-125a-5p to create a ceRNA network in FLSs-RA. The glucose metabolism rate was elevated in FLSs-RA, showing a glucose-dependent characteristic compared to normal FLSs. The enzyme hexokinase 2 (HK2), which is crucial for glucose metabolism, was identified as a direct target of miR-125a-5p in FLSs. In rescue experiments, restoring miR-125a-5p in circFNDC3B-overexpressing FLSs-RA successfully counteracted the circFNDC3B-promoted glucose metabolism and resistance to cell injury. In conclusion, this study highlighted the important roles and molecular mechanisms of circFNDC3B in accelerating glucose metabolism and preventing cell apoptosis in fibroblast-like synoviocytes during rheumatoid arthritis by modulating the miR-125a-5p-HK2 axis. Targeting the circFNDC3B-mediated glucose metabolism pathway could be a promising strategy for rheumatoid arthritis therapy.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00745-3.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"83"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11947371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin inhibits subretinal fibrosis by activating Klotho by miR-126-5p.","authors":"Zhijuan Hua, Qin Zhu, Jingfei Yang, Yuxiang Zheng, Wenchang Yang, Dongli Li, Yixin Cui, Lu Shen, Lingna Rao, Xiaofan Zhang, Ling Yuan","doi":"10.1007/s10616-025-00744-4","DOIUrl":"10.1007/s10616-025-00744-4","url":null,"abstract":"<p><p>Subretinal fibrosis is a main cause of visual loss in patients with neovascular age-related macular degeneration (nAMD), for whom there has been a lack of effective medication. Metformin can improve inflammation and angiogenesis in eye diseases. This study aimed to investigate the mechanism by which metformin inhibits subretinal fibrosis. A subretinal fibrosis cell model was induced by treating human retinal pigment epithelial cells (ARPE-19) with TGF-β1, a subretinal fibrosis mouse model was induced by a laser, and both cells and mice were treated with metformin. Cell proliferation, migration, and invasion were detected by CCK-8, scratch, and Transwell assays. Western blotting and immunofluorescence were used to evaluate protein expression levels, and RT‒qPCR was used to detect gene expression levels. HE and Masson staining were used to observe the morphological changes in retinal and choroidal tissues. Metformin treatment inhibited the TGF-β1-induced proliferation, migration, invasion and epithelial‒mesenchymal transition (EMT) of ARPE-19 cells and effectively ameliorated laser-induced subretinal fibrosis in mice. Mechanistically, metformin inhibits the expression of miR-126-5p, promotes Klotho synthesis, slows the progression of subretinal fibrosis, and miR-126-5p targets and negatively regulates Klotho. Metformin activates Klotho by inhibiting miR-126-5p, thereby reversing TGF-β1-induced ARPE-19 cell EMT and improving laser-induced subretinal fibrosis in mice.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"84"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New mechanism of miR-34a-5p in regulating the biological behavior of osteosarcoma by targeting FoxM1.","authors":"Wenxiang Shen, Xiang Liu, Shengdong Wang, Shaowen Du, Liming Cong, Yulong Ma, Kaishan Ye","doi":"10.1007/s10616-025-00758-y","DOIUrl":"10.1007/s10616-025-00758-y","url":null,"abstract":"<p><p>Osteosarcoma (OS), the most common primary malignant bone tumor in pediatric and adolescent populations, is characterized by significant morbidity and mortality. MicroRNAs (miRNAs) are essential non-coding RNAs that exert pivotal regulatory functions in diverse physiological and pathological processes, including tumorigenesis, disease progression, and drug resistance. The association of miR-34a-5p with osteosarcoma has been documented; However, its underlying mechanisms remain poorly understood.This investigation delineates the impact of miR-34a-5p on the proliferation, invasion, migration, and apoptosis of osteosarcoma cells via in vitro assays, aiming to elucidate the associated mechanisms. Employing up-regulation and knockdown strategies, this study evaluated the roles of miR-34a-5p and FoxM1 in modulating osteosarcoma cell behaviors.These effects were further validated through a rescue experiment, providing robust evidence of the miRNA's impact. Quantitative RT-PCR showed that, compared with normal tissues, miR-34a-5p was significantly downregulated while FoxM1 was markedly upregulated in nine osteosarcoma samples.Increased miR-34a-5p expression attenuated proliferation, migration, and invasion in MG-63 and U2OS cell lines, while enhancing apoptosis.Bioinformatic analyses and dual luciferase assays identified FoxM1 as a downstream target of miR-34a-5p, a finding corroborated by quantitative RT-PCR and Western blotting, which confirmed the negative regulation of FoxM1 by miR-34a-5p.Additionally, FoxM1 knockdown reduced tumor cell proliferation, migration, and invasion, concurrently promoting apoptosis; co-inhibition of miR-34a-5p and FoxM1 partially mitigated these effects. This study demonstrates that miR-34a-5p significantly inhibits osteosarcoma cell proliferation, migration, and invasion, while promoting apoptosis, by targeting and suppressing FoxM1. Our findings suggest that miR-34a-5p is a potential tumor suppressor with therapeutic value. The establishment of the miR-34a-5p/FoxM1 regulatory axis provides new insights into the molecular mechanisms of osteosarcoma. Targeting this axis could offer a promising strategy for improving the prognosis of osteosarcoma.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"90"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12011684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BAP1-mediated ubiquitination inhibition and CAS6/AXL signaling activation in bladder cancer progression.","authors":"Liang Chen, Zhenjun Liu","doi":"10.1007/s10616-025-00757-z","DOIUrl":"10.1007/s10616-025-00757-z","url":null,"abstract":"<p><p>This study investigates the role of BRCA1-associated protein 1 (BAP1) in regulating the ubiquitination of SP1, YAP, and PD-L1, as well as its impact on the CAS6/AXL signaling pathway in bladder cancer progression. Transcriptomic analysis was performed using the GSE3167 dataset to identify key gene expression patterns and regulatory mechanisms. A bladder cancer mouse model was established with control (NC), OE-BAP1, and KD-BAP1 groups to assess the effects of BAP1 overexpression and knockdown. Western blot analysis evaluated the expression levels of BAP1, SP1, YAP, PD-L1, CAS6, AXL, and related signaling proteins. Functional assays, including scratch, Transwell, and colony formation, were conducted to assess cell migratory, invasive, and proliferative capacities. Additional groups included BAP1, SP1 inhibitor, BAP1 + SP1 inhibitor, SP1 + anti-PD-L1 monoclonal antibody, and BAP1 + SP1 + anti-PD-L1 combination to evaluate the interplay of these regulatory mechanisms. BAP1 overexpression significantly increased the expression of SP1, YAP, PD-L1, CAS6, AXL, and downstream signaling proteins (PI3K, STAT3, ERK½, MMP-2, and MMP-9), while BAP1 knockdown reduced their levels. Functional assays showed that the BAP1 group exhibited significantly enhanced migratory, invasive, and proliferative abilities compared to controls. Inhibiting SP1 or combining SP1 inhibition with anti-PD-L1 treatment effectively reduced migration, invasion, and proliferation, particularly after 48 h. BAP1 promotes bladder cancer progression by inhibiting the ubiquitination of SP1, YAP, and PD-L1 and activating the CAS6/AXL signaling pathway. These findings highlight BAP1 as a potential therapeutic target for bladder cancer treatment.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"95"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12050257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: hsa_circ_0000218/hsa-miR-139-3p/SOX4 regulatory feedback circuit influences the proliferation and apoptosis of gastric cancer cells.","authors":"Ganlin Xia, Anxin Wang, Liangxue Li","doi":"10.1007/s10616-025-00747-1","DOIUrl":"10.1007/s10616-025-00747-1","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-021-00509-9.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"108"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12116950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA SNHG25 facilitates colorectal cancer progression by upregulating PPP2R2D expression through sponging miR-329-3p.","authors":"Yuanqiang Li, Weipeng Liu, Chao Liu, Guangsheng Wang, Xin Zhou","doi":"10.1007/s10616-025-00753-3","DOIUrl":"10.1007/s10616-025-00753-3","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) have been evidenced to function as pivotal modulators in tumorigenesis. LncRNA SNHG25 is highly expressed in colorectal cancer (CRC), but its specific function in CRC has not been elucidated yet. The expression of SNHG25, miR-329-3p, and PPP2R2D was determined using qRT-PCR analysis and western blot analysis. The influence of the SNHG25/miR-329-3p/PPP2R2D axis on CRC progression was explored through in vitro assays including CCK-8, colony formation, wound healing, Transwell assays and in vivo orthotopic xenografts assay. The interaction between miR-329-3p and SNHG25 or PPP2R2D was examined by RNA pull-down, RIP, and luciferase reporter assays. SNHG25 presented high expression in CRC cell lines. Silencing of SNHG25 suppressed the malignant phenotypes of CRC cells in vitro and tumor growth in vivo. MiR-329-3p, which displayed low expression in CRC cells, was sponged by SNHG25. Downregulation of miR-329-3p reversed the inhibitory effects of SNHG25 silencing on CRC cell malignant behaviors. Additionally, PPP2R2D served as a miR-329-3p downstream target, whose expression was downregulated by overexpressing miR-329-3p. Importantly, overexpression of PPP2R2D rescued SNHG25 silencing-induced repression on CRC cell malignancy. SNHG25 plays a carcinogenic role in CRC via regulation of the miR-329-3p/PPP2R2D axis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00753-3.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"89"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12008101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-cancer efficiency of <i>Campylobacter jejuni</i> secretome loaded chitosan nanoparticles on colorectal cancer signaling pathways.","authors":"Ghazale Khodadadi, Masoumeh Saberpour, Bita Bakhshi, Sara Minaeian","doi":"10.1007/s10616-025-00756-0","DOIUrl":"10.1007/s10616-025-00756-0","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains as a major health problem with high lethality rate in the world. The innovate therapeutic strategies are essential in CRC management. The purpose of this research was to evaluate the effect of chitosan nanoparticle containing <i>Campylobacter jejuni</i> culture supernatant (CNP/Cj-sup) on genes involved in CRC signaling pathways. CNP/Cj-sup was fabricated via ionotropic gelation method. Dynamic light scattering and transmission electron microscopy (TEM) techniques were employed to characterize of the CNP/Cj-sup including the electrical charge, size distribution, and morphological properties. The loaded protein, released protein, and entrapment efficacy (EE) were assayed utilizing a BCA assay kit. After the evaluation of the viability of Caco-2 (colon adenocarcinoma) and HDF (human dermal fibroblasts) cells against CNP/Cj-sup by MTT assay, subsequently anti-tumor effect of CNP/Cj-sup on genes associated with CRC signaling pathways was assessed via real-time PCR method. The size dispersion of CNP/Cj-sup was 400.6 ± 24.4 nm with an electrical charge of + 4.5 mV. The loaded protein was calculated 1100 µg. The release rate of protein from CNP/Cj-sup was 78% at pH of 6.8 after 48 h, with EE of 74.62%. The viability of Caco-2 and HDF cells against CNP/Cj-sup (1100 µg + 0.05%) was measured 75.8 and 96.5%, respectively after 48 h. CNP/Cj-sup exhibited the highest efficacy in inhibiting the expression of oncogenes <i>TGF-α, Bcl2, TLR4, CEA, TGF-β</i>, and <i>PI3K</i> by to 0.06, 0.34, 0.14, 0.13, 0.08, and 0.14-fold (<i>p</i> value < .0001). Moreover, it led to a significant increase in the expression of the suppressor genes <i>caspase9</i> and <i>PTEN</i> by to 55.7 and 1.8- fold (<i>p</i> value < .0001). CNP/Cj-sup demonstrated the highest efficiency in suppressing <i>TGF-α</i> and enhancing <i>caspase9</i> compared to CNP and Cj-sup. In conclusion, CNP/Cj-sup as an innovative potential anticancer agent, with the ability to modulate genes involved in CRC progression, represents a promising approach to CRC treatment.</p><p><strong>Graphical abstract: </strong>The effect of CNP/Cj-sup on different colorectal cancer signaling pathways.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"93"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression and clinical significance of IGF-1 and PDGF in aqueous humor and serum of diabetic patients with visually significant cataract.","authors":"Minghui Chen, Xiuwen Dai, Jing Liang","doi":"10.1007/s10616-025-00754-2","DOIUrl":"10.1007/s10616-025-00754-2","url":null,"abstract":"<p><p>This study aimed to analyze the expression and clinical significance of IGF-1 and PDGF in the aqueous humor and serum of diabetic patients with visually significant cataract. A retrospective study was conducted on 136 diabetic patients with visually significant cataract who underwent phacoemulsification. Patients were divided into non-complication (n = 82) and complication groups (n = 54) based on postoperative outcomes. Clinical baseline data, as well as IGF-1 and PDGF levels in aqueous humor and serum, were compared between groups. ROC curve analysis was utilized to evaluate the predictive value of IGF-1 and PDGF for postoperative complications. Logistic regression was employed to identify risk factors, and Kaplan-Meier analysis was adopted to assess the impact of IGF-1 and PDGF levels on postoperative complications. No significant differences were found between the two groups in terms of gender, age, BMI, intraocular pressure, surgical eye, phacoemulsification time, phacoemulsification energy, axial length, smoking, drinking history, hypertension, hyperlipidemia, FINS, HbA1C, CRP, or FPG. However, significant differences were observed in disease duration, presence of retinopathy, and IL-6 levels. Patients with complications had significantly higher IGF-1 and PDGF levels in both aqueous humor and serum compared to those without complications. Elevated IGF-1 and PDGF levels were independent risk factors for complications and increased the risk of postoperative complications. Elevated IGF-1 and PDGF levels in aqueous humor and serum are significant independent risk factors for postoperative complications in diabetic patients with visually significant cataract. Both markers can assist in predicting adverse outcomes and are associated with an increased risk of complications.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"94"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12040779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Proanthocyanidin B2 alleviates <i>Pg</i>.LPS-induced RAW264.7 cellular inflammation and oxidative stress via PI3K/Akt/NFkB pathway.","authors":"Xin Chen, Zhichun Fang, Junwei Zhao, Xiaoyan Ou","doi":"10.1007/s10616-025-00751-5","DOIUrl":"10.1007/s10616-025-00751-5","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-025-00734-6.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"91"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12014985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ameliorative potential of metformin in LPS and glutamate-induced neurotoxicity in N2a cell-line.","authors":"Deepshikha, Nikhila Shekhar, Sakshi Tyagi, Ajit Kumar Thakur","doi":"10.1007/s10616-025-00777-9","DOIUrl":"10.1007/s10616-025-00777-9","url":null,"abstract":"<p><p>The study aims to explore the potential of metformin to counteract the lethal effects of glutamate and lipopolysaccharide (LPS)- induced neurotoxicity in Neuro2a (N2a) cells, resembling CNS-comorbidities generally associated with metabolic disorders. Glutamate and LPS-induced N2a cell models were used to conduct the <i>in-vitro</i> study to evaluate the beneficial effect of metformin. Cell viability assay, biochemical parameter viz<i>.</i> cytokines level, superoxide dismutase (SOD) was performed. Further, reactive oxygen species (ROS) were also staged using the Fluorescence-Activated Cell Sorting (FACS) technique to evaluate the beneficial effect of metformin on oxidative stress. Metformin treatments during the study revealed neuroprotective effects and abridged neurotoxicity by significantly reducing the levels of cytokines (viz<i>.</i> IL-1β, IL-6, and TNF-α), raising SOD enzyme activities and declining the ROS levels in LPS and glutamate-treated N2a cells. Based on experimental observation, in an <i>in-vitro</i> study, the effective dose of Met was 50 µM. The results showed that metformin had a neuroprotective effect by enhancing cell viability, diminishing the cytokine storm, and reducing various oxidative stressors. These findings imply that due to the anti-inflammatory, diminishing reactive oxidative species, and antioxidant properties of metformin, it can be considered a therapeutic drug candidate for treating and managing neurological disorders and CNS complications associated with metabolic abnormalities. Further, an <i>in-vivo</i> mechanistic study is warranted to validate the safety and efficacy of metformin for neurological disorders associated with metabolic abnormalities and neurodegenerative disorders.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"107"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}