Cellular Physiology and Biochemistry最新文献

{"title":"Drug Development in Abu Dhabi: Advancing Innovation Through Government Support and a Thriving Ecosystem.","authors":"Namir Shaabani, Aleh Ibrahim Saleh, Mohamed Salem Alameri, Sharukh Hashmi, Tareq Abu Nadi","doi":"10.33594/000000794","DOIUrl":"https://doi.org/10.33594/000000794","url":null,"abstract":"<p><p>Drug development is a complex, high-risk, and resource-intensive process, with global challenges such as high costs, regulatory hurdles, and low clinical trial success rates. These obstacles are especially acute for biotech startups and companies in emerging markets, where access to infrastructure, patient populations, and capital can be limited. This Perspective advocates for Abu Dhabi's emerging life sciences ecosystem as a potential framework for other regions seeking to accelerate pharmaceutical innovation. By offering government-backed incentives, advanced research infrastructure, regulatory support, and access to regional genomic data, Abu Dhabi provides a model for addressing industry bottlenecks and fostering sustainable drug development growth in new markets.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 4","pages":"478-484"},"PeriodicalIF":2.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Magnesium and Zinc Dose-Dependently Stabilize Rat Peritoneal Mast Cells and Enhance the Effects of Adrenaline.","authors":"Itsuro Kazama, Hiroyuki Sonobe, Junko Shida","doi":"10.33594/000000793","DOIUrl":"https://doi.org/10.33594/000000793","url":null,"abstract":"<p><strong>Background/aims: </strong>Magnesium and zinc are vital trace elements found in numerous foods and dietary supplements. In addition to their antioxidant, anticancer, antibacterial, and anti-inflammatory effects, clinical research has suggested that they possess anti-allergic properties.</p><p><strong>Methods: </strong>Using differential-interference contrast (DIC) microscopy, we examined the effects of magnesium chloride (MgCl2) and zinc chloride (ZnCl2) on rat peritoneal mast cell degranulation. We also examined their effects in conjunction with adrenaline, the first-choice drug for anaphylaxis treatment.</p><p><strong>Results: </strong>Both MgCl2 and ZnCl2 reduced the number of degranulating mast cells in a dose-dependent manner. MgCl2 significantly decreased the number of degranulating mast cells at concentrations of 50 mM or higher, whereas ZnCl2 achieved similar effects at much lower concentrations of 25 µM or more. These levels of MgCl2 or ZnCl2 enhanced the inhibitory effects of 1 mM adrenaline on mast cell degranulation. Additionally, pharmacological inhibition of the transient receptor potential cation channel subfamily M member 7 (TRPM7) by NS8593 reduced the number of degranulating mast cells in a dose-dependent manner.</p><p><strong>Conclusion: </strong>This study is the first to provide in vitro evidence that magnesium and zinc stabilize mast cells in a dose-dependent manner and also enhance the effects of adrenaline. TRPM7, which has higher permeability to zinc ions than to magnesium ions, may contribute to the stronger mast cell-stabilizing properties of zinc.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 4","pages":"465-477"},"PeriodicalIF":2.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein Tyrosine Kinase 2 Circular RNA Promotes Proliferation and Invasion of Bladder Cancer.","authors":"Jingyi Cao, Guangyue Wang, Yan Zhao, Guihua Zhang, Qian Wang, Hua Peng, Jie Liang, Jie Zhou, Yuning Dong, Shasha Li, Ke Jiang, Changsong Pei, Qichao Wang","doi":"10.33594/000000792","DOIUrl":"https://doi.org/10.33594/000000792","url":null,"abstract":"<p><strong>Background/aims: </strong>Bladder cancer is a type of malignant tumor that disrupts normal urinary function in patients, thereby significantly impacting their quality of life. This disease also imposes a heavy economic burden on both patients and public health agencies due to high medical costs. Current common therapies, such as surgical intervention, chemical treatment, and radiotherapy, are associated with serious adverse reactions and risks of metastasis recurrence. Effective attenuation of bladder cancer proliferation and invasion remains a significant challenge. Circular RNAs have shown promise in regulating proliferation and migration of cancer cells, thus making it a potential therapeutic target for bladder cancer treatment and prognosis. This study aims to evaluate the impact of regulating circPTK2 expression on progression of bladder cancer.</p><p><strong>Methods: </strong>This research established overexpression and knock down circPTK2 models of bladder cancer cells (SW780 and UM-UC-3) primarily. Then evaluate the effect by a series of cell function test (including RT-qPCR, MTT, EdU assay, cell clone, transwell, cell cycle and cell apoptosis).</p><p><strong>Results: </strong>The findings suggest that regulated expression of circPTK2 in bladder cancer cells correlated with the abundance of mir129-5p. Meanwhile, knock down circPTK2 expression in bladder cancer cells reduced their ability to proliferate and invade; but these processes were reversed when circPTK2 expression was increased.</p><p><strong>Conclusion: </strong>In conclusion, circPTK2 may play a vital role in regulating bladder cancer progression, thereby showing potential for treatment of bladder cancer and improvement of prognosis by modulating circPTK2.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 4","pages":"453-464"},"PeriodicalIF":2.5,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Fat Diet Induces MASLD and Adipose Tissue Changes in Obesity-Resistant Rats.","authors":"Amanda Rangel Madureira, Vinicius Valois Pereira Martins, Janete Corrêa Cardoso, Suellem Torezani-Sales, Kiany de Oliveira Miranda, Breno Souza Salgado, Lidianne Narducci Monteiro, Breno Valentim Nogueira, André Soares Leopoldo, Ana Paula Lima-Leopoldo","doi":"10.33594/000000791","DOIUrl":"https://doi.org/10.33594/000000791","url":null,"abstract":"<p><strong>Background/aims: </strong>Obesity Resistance (OR) is characterized by limited weight gain and reduced fat accumulation despite an obesogenic diet. However, the metabolic risk, particularly regarding Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), remains unclear. The current study aims to investigate the presence of MASLD, as well as metabolic parameters and morphological aspects of adipose tissues in obesity-resistant (OR) R rats fed a high-fat diet (HFD).</p><p><strong>Methods: </strong>ale Wistar rats (n=71) were initially randomized into two groups: a) standard diet (SD, n=35) and b) high-fat diet (HFD, n=36). The protocol was performed for 14 weeks, including 4 weeks of induction and 10 weeks of exposure to obesity. Subsequently, after applying the tertile classification criterion, the animals were redistributed into three groups: a) control (C, n=12), fed a standard diet; b) obesity-prone (OP, n=12); and c) OR (n=12). Body weight evolution, adiposity, nutritional behavior, metabolic markers, and liver morphology were assessed, along with the staging of MASLD.</p><p><strong>Results: </strong>OR rats exhibited lower body weight, total fat pads, and leptin compared to OP but higher values than C. MASLD was observed in 50% of OR animals, while 37.5% progressed to metabolic dysfunction-associated steatohepatitis (MASH). OP rats had a higher incidence of MASH (87.5%).</p><p><strong>Conclusion: </strong>Chronic HFD exposure in OR rats lead to metabolic changes and MASLD development, including MASH, demonstrating that OR does not protect against HFD-induced hepatic alterations.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 4","pages":"434-452"},"PeriodicalIF":2.5,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Roles for Geranylgeranyl Transferase-III (GGTase-III) in Insulin Secretion.","authors":"Noah F Gleason, Mirabela Hali, Anjaneyulu Kowluru","doi":"10.33594/000000783","DOIUrl":"https://doi.org/10.33594/000000783","url":null,"abstract":"<p><strong>Background/aims: </strong>Post-translational prenylation of G proteins is implicated in physiological insulin secretion. It has been reported recently that GGTase-III participates in the functional regulation of Ykt6, a synaptobrevin homolog, <i>via</i> geranylgeranylation. However, potential localization and putative regulatory roles of GGTase-III in insulin secretion remains unknown. The current study is aimed at determining the expression and contributory roles of GGTase-III in glucose- and KCl-induced insulin secretion from pancreatic β-cells.</p><p><strong>Methods: </strong>Mouse islets were isolated by the collagenase digestion method. Human islets were from Prodo Laboratories. INS-1 832/13 cells were transfected with either control (scrambled) or siRNA-PTAR1 (the α-subunit of GGTase-III) using lipofectamine RNAiMax. Insulin released into the medium was quantified using a commercially available Insulin ELISA kit. Expression of GGTase-III subunits and ykt6 was determined by Western blotting and quantified by densitometry.</p><p><strong>Results: </strong>Western blotting revealed that both subunits of GGTase-III (PTAR1 and RabGGTB) are expressed in human islets, mouse islets and INS-1 832/13 cells. Transfection of INS-1 832/13 cells with siRNA-PTAR1 resulted in significant reduction (~50%) in the expression of PTAR1. siRNA-mediated knockdown of PTAR1 significantly attenuated (~60%) glucose-stimulated insulin secretion (GSIS) in INS-1 832/13 cells. Furthermore, insulin secretion elicited <i>via</i> KCl-induced membrane depolarization was markedly reduced (~69%) in INS-1 832/13 cells following PTAR1 depletion. Lastly, immunoblotting data suggested expression of Ykt6, a known substrate for GGTase-III, in human islets, rodent islets, and INS-1 832/13 cells.</p><p><strong>Conclusion: </strong>GGTase-III-dependent signaling step is necessary for glucose- and KCl-induced insulin secretion.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 3","pages":"419-426"},"PeriodicalIF":2.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF-O-Glcnac Axis - Implications for Breast Cancer Metastasis.","authors":"Karolina Anna Kozal, Monika Jarosiewicz, Aleksandra Ewa Szustka, Marek Mądrecki, Marcin Jankowski, Paweł Janusz Jóźwiak, Anna Krześlak","doi":"10.33594/000000782","DOIUrl":"https://doi.org/10.33594/000000782","url":null,"abstract":"<p><strong>Background/aims: </strong>Hypoxia-inducible factor isoforms HIF1 and HIF2 are crucial in the hypoxia response but might also support cancer progression, including breast cancer. O-GlcNAcylation, a post-translational modification regulated by the OGT enzyme, is also emerging as a contributor to breast cancer malignancy. This study aimed to elucidate the role of HIF1 and HIF2 in breast cancer progression and their relationship to O-GlcNAcylation.</p><p><strong>Methods: </strong>We analyzed clinical breast cancer samples, assessing HIF1, HIF2, OGT, and the total O-GlcNAcylation levels by the Western Blot method and their association with clinicopathological characteristics. Additionally, we employed <i>in vitro</i> silencing of OGT, HIF1, and HIF2 in breast cancer cell lines (MCF-7 and MDA-MB-231) to examine their effects on genes expression and cell migration (wound healing assay). A p-value < 0.05 was considered to indicate a statistically significant difference.</p><p><strong>Results: </strong>In breast cancer samples, both HIF isoform levels were elevated in tumors, but HIF2 was associated with lymph node metastasis. A negative correlation was found between HIF2 and O-GlcNAcylation. Silencing HIF2 slowed cell migration, increased O-GlcNAcylation, and decreased the expression of metastasis-related genes. Silencing HIF1 or OGT resulted in the increased expression of these genes, potentially due to increased levels of HIF2.</p><p><strong>Conclusion: </strong>Our findings suggest that the HIF-O-GlcNAc axis plays a critical role in breast cancer progression and metastasis, with HIF1 and HIF2 exhibiting distinct functions.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 3","pages":"404-418"},"PeriodicalIF":2.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inactivation of the Reactive Oxygen Species-Dependent PI3K/Akt/Mtor Signaling Pathway by Phloroglucinol Contributes to Cytotoxicity in Hep3B Human Hepatocellular Carcinoma Cells.","authors":"So Young Kim, Hyun Hwangbo, Gi-Young Kim, Yung Hyun Choi","doi":"10.33594/000000781","DOIUrl":"10.33594/000000781","url":null,"abstract":"<p><strong>Background/aims: </strong>Phloroglucinol is a phenolic derivative isolated from brown algae and reportedly has the potential to induce apoptosis in cancer cells, but its mechanism is unclear. This study aimed to elucidate the complete anticancer mechanism of phloroglucinol in Hep3B human hepatocellular carcinoma (HCC) cells.</p><p><strong>Methods: </strong>We investigated whether phloroglucinol inhibits the proliferation of Hep3B cells by inducing DNA damage and apoptosis, and conducted a study on the mechanism involved. We also explored whether phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is involved in phloroglucinol-induced apoptosis. In addition, we evaluated whether reactive oxygen species (ROS) was involved in the anticancer activity of phloroglucinol.</p><p><strong>Results: </strong>Our results revealed that phloroglucinol disrupted mitochondrial integrity and induced caspase-dependent apoptosis by altering the expression of Bcl-2 family proteins and increasing the cytosolic release of cytochrome <i>c</i> . Phloroglucinol also inactivated the PI3K/Akt/mTOR signaling pathway, and pretreatment with a PI3K inhibitor remarkably augmented the phloroglucinol-induced cytotoxic effect in Hep3B cells. In addition, phloroglucinol significantly stimulated generation of ROS and reduced glutathione ratios. However, a ROS scavenger attenuated phloroglucinol-induced oxidative stress, DNA damage, and apoptosis, thus restoring the reduced cellular viability by blockading phloroglucinol-mediated inactivation of PI3K/Akt/mTOR signaling.</p><p><strong>Conclusion: </strong>Our findings support a mechanism in which phloroglucinol enhances Hep3B cell apoptosis by inactivating the ROS-dependent PI3K/Akt/mTOR pathway, which implies that ROS generation acts as an inducer of phloroglucinol-mediated anticancer activity. Taken together, our findings support further research on the potential of phloroglucinol as a candidate for treating HCC.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 3","pages":"389-403"},"PeriodicalIF":2.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The P53^N236S Mutation Plays a Regulatory Role in Osteosarcoma Metastasis Via the Cholesterol-Hedgehog Pathway.","authors":"Wang Lulin, Liu Jiawei, Zhang Shuojie, Xie Xiaoli, Wang Hui, Jing Jia, Dan Juhua","doi":"10.33594/000000780","DOIUrl":"https://doi.org/10.33594/000000780","url":null,"abstract":"<p><strong>Background/aims: </strong>Osteosarcoma is the most common primary bone cancer affecting children and adolescents worldwide. Although many treatments for osteosarcoma have been explored, the overall survival rate for patients with metastatic osteosarcoma is only 20% due to the lack of understanding of the biological mechanisms by which osteosarcoma metastasis occurs. Therefore, it is important to uncover the molecular mechanism of metastasis in osteosarcoma.</p><p><strong>Methods: </strong>We compared the migration ability of primary osteosarcoma cells from p53 knockout (p53null) and p53^N236S knock-in (p53S) mice. Furthermore, via RNA-sequencing (RNA-seq) data from mouse embryonic fibroblast (MEF) cells, we explored the mechanism by which p53S regulates the cholesterol synthesis pathway and the Hedgehog signaling pathway in primary osteosarcoma cells.</p><p><strong>Results: </strong>We found that the migration ability of primary tumor cells from p53S mice was increased both <i>in vivo</i> and <i>in vitro</i> . Further investigations revealed that the cholesterol content in p53S sarcoma tissue and primary cells was increased following the upregulation of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR). We subsequently observed that elevated cholesterol levels can regulate the Hedgehog (HH) pathway and lead to tumor metastasis. We subsequently treated p53S sarcoma cells with the cholesterol neutralizer methyl-β-cyclodextrin (MβCD) and an HH pathway inhibitor; consequently, we reported that total cholesterol levels reduced both Hedgehog pathway activity and cell migration, whereas HH pathway activity reduced only cell migration.</p><p><strong>Conclusion: </strong>In summary, we confirmed the enhanced metastatic ability of p53S sarcoma primary cells via <i>in vivo</i> and <i>in vitro</i> experiments and preliminarily confirmed the mechanism by which p53S promotes cholesterol synthesis and further activates the HH signaling pathway, thus leading to sarcoma metastasis. This study provides a theoretical basis for further revealing the function and mode of action of p53 mutations in the process of sarcoma metastasis, thereby providing a new potential target for the targeted diagnosis and treatment of sarcoma.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 3","pages":"375-388"},"PeriodicalIF":2.5,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-Mediated Mechanisms of Drug Resistance in Lung Cancer: Molecular Mechanisms and Therapeutic Strategies.","authors":"Vita Havryliuk, Karolina Wojtowicz, Maciej Gagat, Agnieszka Żuryń","doi":"10.33594/000000779","DOIUrl":"https://doi.org/10.33594/000000779","url":null,"abstract":"<p><p>Lung cancer, one of the leading causes of cancer-related deaths globally, is notorious for its poor prognosis and limited response to conventional therapies. Despite advancements in chemotherapy, targeted therapies, and immunotherapy, the efficacy of these treatments is often undermined by the development of resistance, particularly multidrug resistance (MDR). MDR in lung cancer is primarily driven by various mechanisms, including the overexpression of ATP-binding cassette (ABC) transporters like P-glycoprotein (ABCB1), which actively pump chemotherapeutic drugs out of cancer cells, reducing their intracellular concentration and effectiveness. Additionally, genetic mutations, enhanced DNA repair mechanisms, and alterations in drug targets contribute to this phenomenon. The complexity of MDR not only complicates treatment regimens but also contributes to the high mortality rate associated with lung cancer. Understanding the underlying mechanisms of MDR and developing strategies to overcome this resistance are critical for improving patient outcomes. The objective of this review is to present a comprehensive summary of the current knowledge on conventional and emerging mechanisms of drug resistance, with a particular focus on the involvement of exosomes and exosome-mediated factors that mediate drug resistance in lung cancer. Exosomes, tiny vesicles secreted by cells, play a critical role in drug resistance, especially in lung cancer. They carry genetic material and proteins that can alter the behavior of recipient cells, promoting resistance. In lung cancer, exosomes transfer miRNAs and other molecules that enhance survival pathways and inhibit cell death, contributing to chemoresistance. Recent research highlights the potential of targeting exosomal pathways to develop new therapeutic strategies.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 3","pages":"358-374"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of IL4 (Rs2243250) Gene Variant and Mycoplasma Pneumoniae Infection with Asthma Susceptibility in an Iraqi Population.","authors":"Sarah Kassab Shandaway Al-Zamali, Shahad Saad Mohammed, Safa Hasan Radhi, Sara Aqeel Hassan, Ghufran Abd Omran Abdulridha","doi":"10.33594/000000778","DOIUrl":"https://doi.org/10.33594/000000778","url":null,"abstract":"<p><strong>Background/aims: </strong>Asthma is a multifactorial disease influenced by both genetic and environmental factors. This study aimed to investigate the association between the IL4 gene polymorphism (rs2243250) and asthma susceptibility, along with serum IL-4 levels. Additionally, it explored <i>Mycoplasma pneumoniae</i> infection as a potential risk factor for asthma.</p><p><strong>Methods: </strong>A total of 118 individuals were enrolled, including 60 asthma patients and 58 healthy controls. Genotyping for IL4 rs2243250 was performed using allele-specific PCR (AS-PCR). Previous <i>Mycoplasma pneumoniae</i> infection was assessed serologically, and serum IL-4 levels were measured using ELISA.</p><p><strong>Results: </strong>No significant differences were observed between groups in terms of age, sex, or residence. Smoking (OR: 7.85, <i>P</i> = 0.001) and family history of asthma (OR: 5.33, <i>P</i> = 0.004) were identified as significant risk factors. <i>Mycoplasma pneumoniae</i> infection was significantly more prevalent in asthma patients (41.7%) than in controls, with a strong association with asthma risk (OR: 8.75, <i>P</i> < 0.0001). Genotype frequencies of rs2243250 differed significantly: CC (36.7% vs. 68.9%), CT (41.7% vs. 24.2%), and TT (21.6% vs. 6.9%) in patients versus controls, respectively. The T allele was more frequent among patients (42.5%) than controls (18.97%), increasing asthma risk (OR: 3.16, <i>P</i> = 0.0001). Both CT (OR: 3.25) and TT (OR: 5.91) genotypes were strongly associated with asthma. Moreover, individuals with the TT genotype had significantly higher serum IL-4 levels (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>The IL4 rs2243250 polymorphism is associated with increased asthma susceptibility and elevated serum IL-4 levels in the Iraqi population. <i>Mycoplasma pneumoniae</i> infection also appears to be a significant contributing factor. Larger-scale studies are warranted to confirm these findings and further explore the role of this infection in asthma pathogenesis.</p>","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"59 3","pages":"347-357"},"PeriodicalIF":2.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}