Molecular Biology Reports最新文献

{"title":"The importance of phagocytosis and its effect on the immune system.","authors":"Hamra Sude Gençoğlu, Esra Aydemir, Furkan Ayaz","doi":"10.1007/s11033-026-11917-5","DOIUrl":"https://doi.org/10.1007/s11033-026-11917-5","url":null,"abstract":"<p><p>Phagocytosis is a fundamental biological process in the immune system whereby phagocytic cells eliminate pathogens and apoptotic cells. This mechanism plays a central role in ensuring the effectiveness of innate immunity and in activating the antigen recognition and response processes of acquired immunity. This review discusses the importance of phagocytosis in the immune system, its molecular mechanisms, associated disorders, relationship with immunodeficiencies, and its role in vaccine design. In this context, a deeper understanding of phagocytosis may contribute both to improved approaches for the treatment of immunodeficiencies and to the development of next-generation vaccines and immunotherapies.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840006","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":"Neuroprotective effects of black elderberry (Sambucus nigra) extract through the role of miR-124-5p and miR-144-5p in a streptozotocin-induced Type 2 diabetic rat model.","authors":"Arzu Gezer, Fatma Sanlı, Haktan Aslan, Mustafa Özkaraca, Nurcan Kılıç Baygutalp, Ebru Karadağ Sarı, Omer Faruk Karatas, Hilal Üstündağ","doi":"10.1007/s11033-026-11899-4","DOIUrl":"https://doi.org/10.1007/s11033-026-11899-4","url":null,"abstract":"<p><strong>Background: </strong>Type 2 diabetes mellitus (T2DM) leads to neurological complications through multiple pathways. Black elderberry (Sambucus nigra, SN) is rich in bioactive compounds with potential neuroprotective properties. This study sought to evaluate the neural-protective potential of SN extract in STZ-diabetic rats using an integrated molecular, biochemical, and histomorphological approach.</p><p><strong>Methods: </strong>Forty male Sprague-Dawley rats were divided into four groups (n = 10/group): control (C; 0.9% NaCl), SN (0.040 g/kg body weight), diabetes mellitus (DM; streptozotocin 50 mg/kg), and DM + SN (streptozotocin + SN). The treatment period was 10 weeks. Brain tissue was analyzed for histopathological changes, caspase-3 expression, microRNA (miRNA) expression, and oxidative stress markers.</p><p><strong>Results: </strong>Histopathological examination revealed severe neuronal degeneration in the DM group, significantly attenuated in the DM + SN group (p < 0.001). Caspase-3 immunoreactivity was markedly increased in DM group compared to controls and significantly reduced by SN treatment (p < 0.01). In situ hybridization showed high ribonucleic acid (rno)-miR-124-5p and rno-miR-144-5p expression in C and SN groups, with reduced expression in DM group (p < 0.05). SN treatment moderated these changes in DM + SN group. Quantitative real-time polymerase chain reaction (qRT-PCR) confirmed decreased miR-124 expression in DM group, restored to control levels by SN treatment. Biochemically, SN extract reversed diabetes-induced changes in oxidative stress markers, decreasing malondialdehyde (MDA) levels while increasing glutathione (GSH) and nitric oxide synthase (NOS) levels (p < 0.01).</p><p><strong>Conclusions: </strong>SN extract exerted robust neuroprotective actions in the diabetic brain through apoptosis inhibition, miRNA profile restoration, and amelioration of redox imbalance, underscoring its therapeutic promise for diabetes-associated neuropathy.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840023","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":"Research progress on the roles and mechanisms of flavonoid monomers in liver diseases: a review.","authors":"Weijia Zhang, Mi Chen, Chenxia Lu, Li Li, Shupeng Dai, Shengnan Zhang","doi":"10.1007/s11033-026-11901-z","DOIUrl":"https://doi.org/10.1007/s11033-026-11901-z","url":null,"abstract":"<p><p>The liver, a vital metabolic organ with critical roles in detoxification, digestion, and metabolism, is highly susceptible to damage caused by the consumption of alcohol and drugs or infection of viruses. Persistent injury to the liver may progress to severe conditions. Flavonoid monomers, characterized by a fundamental 2-phenylchromone backbone, are a class of traditional Chinese medicine-derived natural polyphenolic compounds. These compounds can inhibit inflammation, oxidation, fibrosis, cancer, and diverse other pathological disorders pharmacologically, which are promising for the treatment of liver diseases. However, the specific mechanisms of flavonoid monomers in liver diseases remain unclear. Based on an extensive literature review, this work summarizes recent research advances on the mechanism of flavonoid monomers in liver diseases. This review is expected to provide novel insights that support the therapeutic application of flavonoid monomers in liver disease treatment.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839985","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 mitochondrial genomes of Iris lactea reveals gene transfer and RNA-editing events.","authors":"Shuqiong Lu, Chunyu Tian, Yanting Yang, Wenlong Gong, Lemeng Liu, Yumei Feng, Zhiyong Li, Jikuan Chai, Zinian Wu","doi":"10.1007/s11033-026-11737-7","DOIUrl":"https://doi.org/10.1007/s11033-026-11737-7","url":null,"abstract":"<p><strong>Background: </strong>As an important perennial herb in the Iridaceae family, Iris lactea shows strong resistance to saline-alkali, drought, and cold stress, possessing significant ecological, medicinal, and economic value. In this study, we assembled the complete mitochondrial genome of I. lactea using whole-genome sequencing data.</p><p><strong>Methods and results: </strong>The assembled genome was 449,819 bp in length (GenBank Accession: PX667947) with a GC content of 46.97%. We found 113 simple sequence repeats, with tetranucleotide motifs being the most common (56, or 49.56%). The genome contains 600 dispersed repeats, consisting of 288 palindromic and 312 forward sequences. This mitogenome contains 36 protein-coding genes with a combined length of 32,343 bp. Analysis of codon usage revealed a strong preference for arginine, leucine, and serine, whereas methionine and tryptophan were infrequently used. We identified 556 RNA-editing sites, all exhibiting cytosine-to-uracil transitions. Analysis of the sequences inserted into the mitochondrial genome revealed that these chloroplast-derived fragments integrated into non-coding IGS regions and rRNA genes.</p><p><strong>Conclusions: </strong>The successful assembly and analysis of the Iris lactea mitogenome significantly enrich the genomic resources of the genus Iris, providing a solid foundation for future research on phylogenetic evolution, germplasm conservation, and genetic improvement of this genus.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840192","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":"Curcumin as a ceramide metabolism-targeting agent: Molecular mechanisms and therapeutic implications in cancer.","authors":"Sajad Dehnavi, Mahvash Sadeghi, Kianush Charoghdoozi, Prashant Kesharwani, Amirhossein Sahebkar","doi":"10.1007/s11033-026-11905-9","DOIUrl":"https://doi.org/10.1007/s11033-026-11905-9","url":null,"abstract":"<p><p>Curcumin, a lipophilic polyphenol widely used in traditional medicine, is the active ingredient in turmeric (Curcuma longa L.). It has various therapeutic effects, such as antitumor potential, due to its interaction with intracellular and extracellular molecules associated with different malignancies. Ceramides are fundamental constituents of cellular membranes that maintain the stability and integrity of cells. Additionally, they have become key signaling agents that govern a spectrum of cellular functions, such as differentiation, proliferation, apoptosis, and cellular senescence. This review primarily introduces ceramides and their metabolism, summarizes their crucial roles in cancer, and categorizes and discusses the mechanisms and pathways through which curcumin could potentially exert its antitumor effects by targeting ceramides. These mechanisms include apoptosis- and autophagy-associated pathways, de novo ceramide generation, and influencing intracellular free calcium levels and acid inhibition. ceramidase, and combinational strategies using various chemical agents, ceramides, or ceramide analogs to enhance curcumin's efficacy. Finally, the review concludes with remarks and prospects for the future of curcumin's antitumor potential in the context of ceramide targeting.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840213","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":"Targeting the APE1 hub: integrating DNA repair and redox signaling for precision management of inflammation-associated diseases.","authors":"Peilan Xu, Peng Zhou, Jia Luo, Yun Liu, He Xiao, Jia Du, Mengxia Li, Chuan Chen","doi":"10.1007/s11033-026-11898-5","DOIUrl":"https://doi.org/10.1007/s11033-026-11898-5","url":null,"abstract":"<p><p>Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional protein that occupies a key position at the interface between base excision repair (BER) and cellular redox control during inflammation. As the major AP endonuclease in the BER pathway, APE1 maintains the genomic stability by the repairing oxidative DNA lesions that accumulate in chronically inflamed tissues. In addition, its redox effector factor 1 (Ref-1) activity modulates a broad range of transcription factors, thereby influencing inflammatory cytokine production and the cellular response to redox imbalance. Through this combination of DNA repair and redox-signaling functions, APE1 acts as a central hub that couples oxidative DNA damage to inflammatory signaling networks. Dysregulation of APE1 expression or subcellular distribution has been associated with various inflammation-associated diseases, reflecting its broad impact on inflammatory pathology. This review summarizes current understanding of APE1's dual role in inflammation, highlights opportunities and challenges for therapeutic targeting, and discusses its emerging value in the precision monitoring and management of inflammation‑associated diseases.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839973","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":"Correction: The Dual Roles of TIMP-1 in Cancer: From Protease Inhibition to Cytokine Signaling.","authors":"Haixia Li, Xinzhou Deng, Fang Wang, Yanlin Niu, Pengfei Ruan, Li Gong, Ming Luo, Zhiguo Luo, Nan Cao","doi":"10.1007/s11033-026-11897-6","DOIUrl":"https://doi.org/10.1007/s11033-026-11897-6","url":null,"abstract":"","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840197","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":"Neuronal deletion of PDE7A averts morphine-induced behavioral plasticity and impairs downstream AKT signaling.","authors":"Zizhen Liu, Axiang Li, Chengyou Zheng, Ruyan Gao, Kaiwu He, Zhen Tan, Tahir Ali, Liangliang Hao, Tao Li, Shupeng Li","doi":"10.1007/s11033-026-11908-6","DOIUrl":"https://doi.org/10.1007/s11033-026-11908-6","url":null,"abstract":"<p><strong>Background: </strong>Phosphodiesterase 7 A (PDE7A) is a key regulator of cyclic adenosine monophosphate (cAMP) signaling, expressed prominently in brain regions associated with reward and addiction. Despite its strategic localization within reward-related neurocircuitry, the functional contribution of PDE7A to substance use disorders remains poorly defined.</p><p><strong>Methods: </strong>We investigated the role of PDE7A in morphine-induced behavioral plasticity using a combination of genetic deletion (Nestin-Cre-mediated neuronal PDE7A knockout) and pharmacological inhibition (BRL-50481) in male C57BL/6J mice (8-10 weeks of age). Behavioral assessments included conditioned place preference (CPP) and locomotor sensitization. Biochemical analyses (ELISA, Western blotting, co-immunoprecipitation) were performed on striatal tissue to assess dopamine levels, cAMP levels, and signaling pathways (AKT/GSK3β, D2R-β-arrestin2 complex).</p><p><strong>Results: </strong>Mice with neuronal PDE7A deficiency failed to develop morphine-induced CPP, highlighting a critical requirement for PDE7A in drug-associated memory formation. Consistently, administration of the PDE7 inhibitor BRL-50,481 (10 mg/kg, i.p.) significantly disrupted established drug memories and attenuated morphine-induced behavioral sensitization in wild-type mice. Mechanistically, PDE7A deletion led to a hyper-dopaminergic state in the striatum, characterized by elevated dopamine levels and D1 receptor expression, yet a paradoxical impairment in downstream signaling. Specifically, the behavioral effects of PDE7 inhibition were reversed by the D2 receptor antagonist haloperidol and the AKT inhibitor oridonin, suggesting a reliance on the D2R-AKT-GSK3β axis. Biochemical analyses further revealed that PDE7A deficiency suppresses the AKT/GSK3β signaling pathway, a defect validated through pharmacological manipulation of PDE7, D2R, and AKT.</p><p><strong>Conclusion: </strong>Collectively, these findings identify PDE7A as a pivotal modulator of morphine-induced addiction and suggest that targeting the PDE7A-D2R-AKT signaling cascade represents a novel therapeutic strategy for managing substance use disorders.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839999","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":"Exploratory study of DEFB1 genetic variants and human β-defensin-1 expression in monosodium urate crystal-induced arthritis: insights into innate immune regulation.","authors":"Javier Fernández-Torres, Karina Martínez-Flores, Ambar López-Macay, Yessica Zamudio-Cuevas","doi":"10.1007/s11033-026-11919-3","DOIUrl":"https://doi.org/10.1007/s11033-026-11919-3","url":null,"abstract":"<p><strong>Background: </strong>Gout is an inflammatory arthritis triggered by the deposition of monosodium urate crystals and characterized by activation of innate immune pathways. Human β-defensin-1 (hBD-1), encoded by the DEFB1 gene, is an antimicrobial peptide with immunomodulatory functions. However, its role in gout-related inflammation remains unclear. This study aimed to investigate the relationship between DEFB1 variants (rs11362 and rs1800972) and circulating hBD-1 levels in gout.</p><p><strong>Methods: </strong>A total of 81 individuals were enrolled, including 41 with gout and 40 healthy controls. Serum hBD-1 concentrations were quantified by ELISA, and genotyping was performed using TaqMan assays. Genetic associations were evaluated using logistic and linear regression models adjusted for relevant metabolic variables. An ANCOVA was performed to compare hBD-1 levels across genotypes, adjusting for age, serum urate, and triglyceride levels.</p><p><strong>Results: </strong>Serum hBD-1 levels were significantly lower in individuals with gout compared with controls (median 34.9 vs. 79.3 pg/mL, p < 0.0001). The rs11362 AA genotype was more frequent among controls and was associated with lower odds of gout across multiple inheritance models after adjustment (p < 0.05). In the overall cohort, this genotype was also associated with higher circulating hBD-1 concentrations (p < 0.0001). This association remained significant after adjusting for covariates in ANCOVA (p < 0.001). No significant associations were observed for the rs1800972 variant.</p><p><strong>Conclusion: </strong>These results suggest that variation in the DEFB1 gene may be associated with differences in hBD-1 expression and gout status. The results provide preliminary evidence that supports a possible link between defensin-related innate immune regulation and gout-associated inflammation. However, given the exploratory design and limited sample size, these results should be interpreted as hypothesis-generating rather than confirmatory. Further studies in larger, well-characterized cohorts are needed to confirm these results and clarify their immunological relevance.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840205","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":"Metabolic reprogramming and ferroptosis in keloid pathogenesis: new insights for targeted therapy.","authors":"Dongxian Lin, Li Duan, Yuanyuan Xu, Shunbing Lu, Chenhao Ma, Yuchen Zhang, Bincheng Wang, Yue Liu, Shanbaga Zhao, Lianzhao Wang","doi":"10.1007/s11033-026-11896-7","DOIUrl":"https://doi.org/10.1007/s11033-026-11896-7","url":null,"abstract":"<p><p>Keloids are persistent fibroproliferative scars with an incompletely understood pathogenesis, traditionally linked to pathways such as TGF-β signaling and chronic inflammation. This review synthesizes recent literature focusing on the emerging roles of metabolic reprogramming and ferroptosis resistance in keloid fibroblasts. Recent studies highlight the convergence of these two processes as central factors sustaining the persistence and therapeutic resistance of these cells. Keloid fibroblasts exhibit cancer-like metabolic reprogramming, marked by a shift toward aerobic glycolysis, mitochondrial dysfunction, and disrupted lipid metabolism. This metabolic reorganization not only reflects the fibrotic process but also serves as a key driver of the fibroblasts' hyperproliferative, invasive, and matrix-producing characteristics. Concurrently, these fibroblasts display significant resistance to ferroptosis, an iron-dependent regulated cell death mechanism, acting as a critical survival strategy. Mechanistically, enhanced glycolysis supplies the reducing equivalents required to sustain the GPX4 antioxidant system, thereby preventing ferroptosis by neutralizing lipid peroxidation. Recognizing this integrated metabolic-ferroptotic axis shifts the therapeutic paradigm from symptomatic management to targeted, mechanism-based strategies. Interventions targeting critical nodes, such as glycolytic enzymes, or inducing ferroptosis with agents like ALA-PDT, present promising approaches to dismantle the survival advantages of keloid fibroblasts. These novel strategies offer the potential for more durable disease control, providing a foundation to overcome current translational challenges in drug delivery.</p>","PeriodicalId":18755,"journal":{"name":"Molecular Biology Reports","volume":"53 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839972","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}