Cell Journal最新文献

{"title":"Dysregulated Acetate Metabolism and Cholesterol Biosynthesis in Cumulus Cells of Women with Polycystic Ovary Syndrome.","authors":"Zahra Safaeinejad, Ali Valipour Motlagh, Fatemeh Razavi, Maryam Esmaeili, Parsa Rezvanian, Rasool Ghaedi-Heydari, Atefeh Ghaderi Khorasgani, Sama Dastjerdi, Mohammad Hossein Nasr-Esfahani","doi":"10.22074/cellj.2026.2077358.1968","DOIUrl":"https://doi.org/10.22074/cellj.2026.2077358.1968","url":null,"abstract":"<p><strong>Objective: </strong>Polycystic ovary syndrome (PCOS) is associated with metabolic disturbances within the follicular microenvironment that may impair oocyte competence. Although elevated acetate levels have been reported in the follicular fluid (FF) of PCOS patients, its metabolic fate and transcriptional impact in cumulus cells (CCs) remain unclear. This study investigated acetate-related metabolic reprogramming in CCs of women with PCOS.</p><p><strong>Materials and methods: </strong>In this experimental study, FF acetate, glucose, and cholesterol levels were measured in 25 PCOS and 15 control women. Transcriptomic analysis of CCs was performed using RNA-seq dataset GSE155489 (discovery cohort with n=2 PCOS; n=2 controls) and independently validated in microarray dataset GSE10946. Differentially expressed genes (DEGs) were identified using platform-specific pipelines. Functional enrichment and protein-protein interaction (PPI) analyses were conducted to identify key metabolic pathways and hub genes. Selected genes were validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in CCs obtained from 30 PCOS and 20 control subjects.</p><p><strong>Results: </strong>FF from PCOS women exhibited significantly increased acetate and cholesterol levels and decreased glucose levels compared with the controls (P<0.001). Transcriptomic analysis identified 665 DEGs in PCOS CCs. Enrichment analyses revealed significant dysregulation of acetate metabolism, tricarboxylic acid (TCA) cycle, and cholesterol biosynthesis pathways. <i>ACSS1</i> and <i>ACSS2</i> were upregulated in PCOS CCs. Hub gene analysis identified <i>PDHA1</i> and <i>IDH1</i> (TCA cycle), and <i>ACLY, HMGCS1,</i> and <i>MVD</i> (cholesterol biosynthesis). RT-qPCR confirmed upregulation of <i>ACSS1, ACSS2, ACLY, HMGCS1</i>, and <i>MVD</i>, and downregulation of IDH1, while <i>PDHA1</i> showed increased expression in the clinical cohort. Correlation analyses demonstrated modest associations between acetate-related genes and certain assisted reproductive technologies (ART) parameters.</p><p><strong>Conclusion: </strong>Congenital hypothyroidism disrupts hormonal balance, increases oxidative stress, and induces ovarian histological alterations. Treadmill training exerts protective effects, highlighting its potential as a non-pharmacological strategy that could mitigate reproductive complications associated with hypothyroidism.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-14"},"PeriodicalIF":2.0,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Treadmill Training on Ovarian Alterations in A Rat Model of Congenital Hypothyroidism.","authors":"Amir Esmaeilnejad Moghaddam, Mobina Molla, Moslem Mohammadi, Zohreh Zare","doi":"10.22074/cellj.2026.2070544.1913","DOIUrl":"https://doi.org/10.22074/cellj.2026.2070544.1913","url":null,"abstract":"<p><strong>Objective: </strong>Thyroid hormones are essential for fetal development, and maternal hypothyroidism may cause reproductive abnormalities in offspring. Physical activity may provide therapeutic benefits. This study investigated the effects of treadmill training on gonadotropin levels, oxidative stress biomarkers, and ovarian histopathological changes in postpubertal rat offspring with congenital hypothyroidism.</p><p><strong>Materials and methods: </strong>In this experimental study, congenital hypothyroidism was induced by administering propylthiouracil in the drinking water of pregnant Wistar rats from gestational day 6 to postnatal day 28. Female offspring were subsequently assigned to four groups (n=7/group): control, control with treadmill training, hypothyroid, and hypothyroid with treadmill training. Rats underwent treadmill training for 4 weeks (5 days/week, 30 minutes/session), with running speed increasing from 2-4 m/minutes during the first 2 weeks to 2-8 m/minutes during the final 2 weeks. After the final training session, blood and ovarian tissues were collected. Serum thyroid hormones and gonadotropins were measured using ELISA kits. In ovarian tissue, follicles were assessed using H and E staining; malondialdehyde (MDA) and glutathione (GSH) levels were measured spectrophometrically, and superoxide dismutase (SOD) and catalase (CAT) activities were determined using commercial assay kits.</p><p><strong>Results: </strong>Hypothyroidism significantly reduced serum thyroid hormones and gonadotropins. It was associated with increased oxidative stress, characterized by elevated MDA levels, decreased GSH levels, and reduced SOD and CAT activities, accompanied by a significant reduction in the number of growing ovarian follicles. Treadmill training ameliorated ovarian alterations in hypothyroid offspring by attenuating oxidative stress and enhancing antioxidant defenses, indicated by a 29% reduction in MDA levels, a 47% increase in GSH levels, and 37% and 51% increases in SOD and CAT activities, respectively.</p><p><strong>Conclusion: </strong>Congenital hypothyroidism disrupts hormonal balance, increases oxidative stress, and induces ovarian histological alterations. Treadmill training exerts protective effects, highlighting its potential as a non-pharmacological strategy that could mitigate reproductive complications associated with hypothyroidism.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-11"},"PeriodicalIF":2.0,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative Analysis of ACTL7A Expression, Localization, and Sperm Functional Parameters in Fertile and Infertile Men: A Case-Control Study.","authors":"Sajedeh Sadat Nourian Najafabadi, Marziyeh Tavalaee, Nushin Naderi, Zahra Fatehi, Yeganeh Karimi, Parnia Zehtab, Rana Zamani, Mohammad Hossein Nasr-Esfahani","doi":"10.22074/cellj.2026.2078738.1974","DOIUrl":"https://doi.org/10.22074/cellj.2026.2078738.1974","url":null,"abstract":"<p><strong>Objective: </strong>Testis-specific actin-like 7A (ACTL7A) is an acrosome/perinuclear-theca-related protein implicated in male infertility. In this exploratory study, we assessed <i>ACTL7A</i> transcript levels in a clinical assisted reproductive technology (ART) setting and performed preliminary protein-level validation in a subset of samples, together with sperm chromatin integrity assays, to clarify potential associations with sperm quality.</p><p><strong>Materials and methods: </strong>For this preliminary case-control study, twenty-seven men were included: 11 infertile intracytoplasmic sperm injection (ICSI) candidates and 16 fertile preimplantation genetic testing (PGT) candidates. <i>ACTL7A</i> mRNA levels were quantified in all samples by quantitative real time polymerase chain reaction (qRTPCR). ACTL7A protein expression was evaluated by Western blot in a small feasibility-limited subset (n=3 per group) and interpreted as exploratory protein-level support for the mRNA findings. Localization was assessed by immunostaining. Classical semen parameters and sperm functional assays including DNA fragmentation (SCSA), histone retention (aniline blue), and protamine deficiency (CMA3) were performed. Clinical outcomes were also documented.</p><p><strong>Results: </strong><i>ACTL7A</i> mRNA levels were significantly reduced in infertile men compared with fertile controls (qPCR: P=0.020). Preliminary Western blot analysis in the subset also suggested lower protein expression in the infertile group (P=0.010), providing supportive evidence for the transcript findings. Infertile men also showed lower sperm viability and poorer chromatin integrity (P=0.040 and P=0.020, respectively). <i>ACTL7A</i> expression positively correlated with sperm viability (r=0.40, P=0.040) and inversely correlated with DNA fragmentation (r=-0.43, P=0.020). Exploratory receiver operating characteristic (ROC) analysis showed a moderate discriminatory ability for <i>ACTL7A</i> expression [area under the curve-ROC (AUC-ROC=0.727, P=0.048], with 62.5% sensitivity and 81.8% specificity.</p><p><strong>Conclusion: </strong>Reduced <i>ACTL7A</i> expression in human sperm is linked to impaired chromatin quality and decreased viability, supporting <i>ACTL7A</i> as a candidate research biomarker rather than a clinically validated predictor. Given the small cohort and limited protein-level testing, these findings are exploratory and emphasize the need for validation in larger independent populations to confirm clinical utility.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-12"},"PeriodicalIF":2.0,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148649568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MCT4-Mediated Metabolic Reprogramming in Tumor-Associated Macrophages Promotes Hepatocellular Carcinoma Progression.","authors":"Zhiying Li, Ni Zhang, Renjie Li, Ying Qi, Yalei Wang, Meng Zhao, Shuo Qie","doi":"10.22074/cellj.2026.2063702.1876","DOIUrl":"https://doi.org/10.22074/cellj.2026.2063702.1876","url":null,"abstract":"<p><strong>Objective: </strong>RMonocarboxylate transporter protein 4 (MCT4), encoded by the <i>SLC16A3</i> gene, mediates lactate efflux into the extracellular microenvironment. This study aimed to characterize the MCT4 overexpression in tumor-associated macrophages (TAMs) at the single-cell level in hepatocellular carcinoma (HCC) and to investigate its role in HCC progression through metabolic reprogramming of TAMs.</p><p><strong>Materials and methods: </strong>In this experimental study, R software and multiple public databases, including UALCAN, TIMER2.0 and TISCH2, were used to analyze <i>SLC16A3</i> expression at the single-cell level and its association with HCC prognosis. <i>In vitro</i> experiments were conducted and <i>SLC16A3</i> knockdown was achieved using shRNAs. TAM polarization was evaluated by Western blot, quantitive real time-polymerase chain reaction (qRT-PCR) and flow cytometry. Additional bioinformatic analyses, including protein-protein interaction (PPI) network analysis, were conducted using STRING to investigate the association between <i>SLC16A3</i> expression and key glycolysis genes.</p><p><strong>Results: </strong>Analysis of the GEO database GSE166635 demonstrated that MCT4 expression was significantly higher in macrophages than in other immune cell populations in HCC. Immunofluorescence (IF) revealed co-localization of MCT4 with the M2 TAM marker CD163. Western blot demonstrated that <i>SLC16A3</i> knockdown reduced CD163 expression at protein levels to 84.1% ± 5.0% (KD-1) and 44.6% ± 8.4% (KD-3) compared to control. Flow cytometry further demonstrated that SLC16A3 knockdown increased the proportion of CD86-positive cells from approximately 13.5% (Con sh) to 43.3% (KD-1) or 43.8% (KD-3), whereas the proportion of CD163-positive cells decreased to approximately 38.2% (KD-1) or 33.4% (KD-3). Survival analysis was performed on HCC patients from TIMER2.0, including 371 HCC patients with complete survival information, further indicated that high SLC16A3 expression combined with increased M2 TAM infiltration was associated with poorer prognosis (P=0.008).</p><p><strong>Conclusion: </strong>High MCT4 expression in TAMs may be associated with metabolic reprogramming toward glycolysis, and could promote M2 polarization of TAMs, thereby contributing to HCC progression and poor clinical outcomes.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-13"},"PeriodicalIF":2.0,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148649640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In APP/PS-1 Transgenic Mice and Aβ-Induced P12 Cell Models, <i>ADCYAP1</i> Inhibits Neuronal Apoptosis and Autophagy, Thereby Alleviating The Pathology of Alzheimer's Disease.","authors":"Yuxi Jiang, Tianrun Yang","doi":"10.22074/cellj.2026.2045830.1718","DOIUrl":"https://doi.org/10.22074/cellj.2026.2045830.1718","url":null,"abstract":"<p><strong>Objective: </strong>Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly. ADCYAP1 encodes pituitary adenylate cyclase activating polypeptide (PACAP), which can exert neuroprotective effects in neurodegenerative diseases. This study aims to probe the specific function of <i>ADCYAP1</i> in AD.</p><p><strong>Materials and methods: </strong>In this experimental study, brain tissue samples from AD patients and healthy controls were collected to assess ADCYAP1 expression. APP/PS-1 transgenic mice were utilised as an AD mouse model along with amyloid beta (Aβ)-induced PC12 cells as an AD cell model. <i>ADCYAP1</i> expression in the AD mice was determined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. An IF assay was employed to test Aβ deposition and microtubule-associated protein 2 (MAP2) expression (a neuron marker). Behavioural tests, including the Morris water maze (MWM) and footprint tests, were performed to evaluate cognitive impairment and motor ability. Cell apoptosis was determined using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-nick end labelling (TUNEL) assay. Western blot was utilised to test the expression of autophagy-related genes, including LC3 and beclin1. The expressions of transcription factors involved in neuronal differentiation was assessed by RTqPCR.</p><p><strong>Results: </strong><i>ADCYAP1</i> expression was significantly downregulated in the brain tissues of AD patients and mice. ADCYAP1 overexpression reduced Aβ deposition and enhanced MAP2 expression in the AD mice. <i>ADCYAP1</i> overexpression effectively improved cognitive impairment and mobility decline in the AD mice. <i>ADCYAP1</i> upregulation inhibited neuronal apoptosis and autophagy both in vivo and in vitro. <i>ADCYAP1</i> upregulated the expression of neuronal differentiationrelated factors [transforming growth factor β (TGFβ), early growth response 1 (Egr1), brain-derived neurotrophic factor (BDNF), fibroblast growth factor 21 (FGF21), and insulin-like growth factor 1 (Igf1)] in the AD models.</p><p><strong>Conclusion: </strong><i>ADCYAP1</i> inhibits neuronal apoptosis and autophagy to improve AD progression in APP/PS-1 mice and Aβ-induced P12 cells.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-13"},"PeriodicalIF":2.0,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148649646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conditioned Medium from Muramyl Dipeptide-Primed Mesenchymal Stem Cells Enhances Therapeutic Efficacy in Experimental Rheumatoid Arthritis.","authors":"Sayed Amin Mirdamadian, Seyyed Meysam M Abtahi Froushani","doi":"10.22074/cellj.2026.2059818.1852","DOIUrl":"https://doi.org/10.22074/cellj.2026.2059818.1852","url":null,"abstract":"<p><strong>Objective: </strong>Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes joint inflammation, disability, and reduced quality of life. Current mesenchymal stem cell (MSC) therapies face limitations due to cell variability and lack of standardization, highlighting the need for effective, cell-free alternatives that replicate MSCs' immunomodulatory functions. This study aimed to enhance MSC secretion of regulatory factors to modulate inflammation in an RA model.</p><p><strong>Materials and methods: </strong>In this experimental study, MSCs were isolated from mouse bone marrow and characterized by CD73 expression and lack of CD45/CD80. MSCs were treated with Muramyl dipeptide (MDP; 0 and 10 μg/mL) for 24 hours, followed by washing and further culture for 48 hours to obtain conditioned medium (CM). The resulting CM from untreated MSCs and MDP-primed MSCs (MDP-CM) was collected for subsequent <i>in vivo</i> administration. RA was induced in male Wistar rats (160-180 g) via intradermal injection of Freund's complete adjuvant. Treatments with CM derived from either untreated MSCs or MDP-pulsed MSCs (MDP-CM) were initiated on day 7 post-induction and repeated after 5 days via intraperitoneal injection (n=10 per group).</p><p><strong>Results: </strong>MDP did not affect MSC viability but significantly altered the CM's immunological profile: MDP-CM had lower levels of IFN-γ, IL-6, and IL-1β, and higher levels of indoleamine 2,3-dioxygenase, TGF-β, and IL-10 compared to control CM. <i>in vivo</i> administration of MDP-CM significantly attenuated RA severity and promoted body weight recovery more effectively than CM alone. In addition, MDP-CM significantly reduced systemic inflammatory markers , such as TNF-α, IL-1β, myeloperoxidase, nitric oxide, and C-reactive protein (CRP), and more strongly modulated T-cell- associated gene expression in joint tissue, evidenced by upregulation of FOXP3 and downregulation of <i>T-bet, Gata3,</i> and <i>Rorc</i> compared with RA rats receiving CM.</p><p><strong>Conclusion: </strong>The CM derived from appropriately primed MSCs may represent a more potent and standardized \"off-theshelf\" alternative to direct stem cell transplantation.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-9"},"PeriodicalIF":2.0,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148346962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum : A Novel Insight into Endothelial and Cardiac Cells Phenotype in Systemic Sclerosis Using Patient-Derived.","authors":"Sedigheh Gholami, Zahra Mazidi, Sara Pahlavan, Fariba Moslem, Mahya Hosseini, Adeleh Taei, Mahdi Hesaraki, Maryam Barekat, Nasser Aghdami, Hossein Baharvand","doi":"10.22074/cellj.2026.735329","DOIUrl":"https://doi.org/10.22074/cellj.2026.735329","url":null,"abstract":"<p><p>In the article published in Cell J, Vol 23, No 3, 2021, pages 273-287, Figure 2H panel (S2-EC/CD31-DAPI)<br>inadvertently contains an image that originally appeared in a 2016 Biomaterials paper previously published by this<br>team (doi: 10.1016/j.biomaterials.2016.01.025). The correct figure is provided below.<br>The authors sincerely apologize for this inconvenience.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-2"},"PeriodicalIF":2.0,"publicationDate":"2026-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Verification of Key Genes Underlying Methamphetamine Sensitization Using Network-Based Analysis.","authors":"Ali Mohammadian, Afsaneh Mokaram Bakhtajerdi, Zahra Mortezaei","doi":"10.22074/cellj.2024.2018281.1470","DOIUrl":"https://doi.org/10.22074/cellj.2024.2018281.1470","url":null,"abstract":"<p><strong>Objective: </strong>Methamphetamine (METH) is a highly addictive psychostimulant that alters gene expression in brain reward circuits. This study aimed to identify METH-associated transcriptional changes in the nucleus accumbens (NAc) and explore potential pharmacological interventions.</p><p><strong>Materials and methods: </strong>We conducted an <i>in silico</i> analysis of publicly available microarray data (GSE46717) from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were identified using limma and analyzed for functional enrichment via EnrichR. Protein-protein interaction (PPI) networks were constructed using STRING to identify hub genes, validated <i>in silico</i> with jackknife resampling. Adult male Wistar rats were injected with METH (10 mg/ kg, followed by 2.5 mg/kg after one month), and expression of selected hub genes was measured in NAc tissue using quantitative polymerase chain reaction (qPCR). Connectivity mapping was applied to identify candidate drugs reversing METH-induced transcriptional changes.</p><p><strong>Results: </strong>We identified 280 DEGs (210 upregulated, 70 downregulated). Upregulated pathways included caffeine metabolism, long-term potentiation, and cocaine addiction, whereas GABAergic and glutamatergic synapse genes were downregulated. Network analysis highlighted Fos, Crh, Oprl1, and Slc17a6 as hub genes, validated both computationally and experimentally. Connectivity mapping identified D-64131 and Mebendazole as potential therapeutics.</p><p><strong>Conclusion: </strong>METH induces substantial transcriptional alterations in the NAc, affecting synaptic signaling and addiction pathways. Integrating <i>in silico</i> network analysis with experimental validation identified robust hub genes and suggested candidate compounds for therapeutic intervention.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-9"},"PeriodicalIF":1.7,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148260299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory T Lymphocyte-Derived Extracellular Vesicles Play A Role in Chronic Kidney Diseases and Kidney Transplantation: A Review.","authors":"Reza Hajiasghar-Sharbaf, Esmaeil Atashbasteh, Hamed Fouladseresht, Nahid Eskandari","doi":"10.22074/cellj.2026.2065015.1884","DOIUrl":"https://doi.org/10.22074/cellj.2026.2065015.1884","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) significantly affects kidney function, often leading to end-stage kidney disease (ESKD). Due to its high rates of morbidity, mortality, and economic effects, CKD is becoming the ninth most important risk factor for mortality worldwide, presenting serious healthcare issues. Regulatory T lymphocytes (Tregs) play a role in regulation, particularly in transplant tolerance and autoimmune conditions. Recent research has highlighted the potential of Tregderived vehicles (EVs) to modulate responses and promote graft tolerance during kidney transplantation. These EVs can suppress effector T lymphocytes (T effect), trigger apoptosis, and modify cytokine production to maintain balance and prevent graft rejection. Moreover, Treg-EVs have emerged as potential biomarkers for diagnosing CKD, paving the way for new diagnostic and therapeutic strategies. This study explores how Treg-derived EVs influence processes underlying CKD and kidney transplantation, highlighting their significance as useful tools.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-9"},"PeriodicalIF":1.7,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148260334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on: miR-129-5p Modulates Fndc5 Expression in Adipose Tissue of Diabetic Mice.","authors":"Baharuddin Baharuddin, Lilies Handayani, Maher Monir Akl","doi":"10.22074/cellj.2026.2086933.2014","DOIUrl":"https://doi.org/10.22074/cellj.2026.2086933.2014","url":null,"abstract":"<p><p>A study demonstrated that increased miR-129-5p expression is associated with reduced Fndc5 expression in adipose tissue of a type 2 diabetes mellitus (T2DM) mouse model, suggesting a post-transcriptional regulatory mechanism contributing to metabolic dysfunction. This Letter discusses the strengths and limitations of these findings. Although the dual-luciferase assay provided strong evidence of a direct interaction between miR-129-5p and the <i>Fndc5</i> 3'UTR, the absence of <i>in vivo</i> loss-of-function or gain-of-function experiments limits causal interpretation. In addition, downstream metabolic consequences of reduced FNDC5/irisin signaling, including insulin signaling pathways, GLUT4 regulation, and thermogenic activity, were not comprehensively evaluated. Methodological concerns, including sample size and the lack of reported blinding procedures, may also affect reproducibility. Future studies integrating miRNA manipulation strategies, circulating irisin measurement, and pathway-based metabolic analyses are needed to strengthen the biological and translational relevance of the miR-129-5p-FNDC5 axis in T2DM.</p>","PeriodicalId":49224,"journal":{"name":"Cell Journal","volume":"28 1","pages":"1-2"},"PeriodicalIF":1.7,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148260218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}