Cell Biochemistry and Function最新文献

{"title":"Brain Involvement in Leishmaniasis","authors":"Camila S. Freitas,&nbsp;Eduardo A. F. Coelho,&nbsp;Myron Christodoulides","doi":"10.1002/cbf.70209","DOIUrl":"10.1002/cbf.70209","url":null,"abstract":"<p>Leishmaniasis is a neglected tropical disease caused by infection with the protozoan parasite <i>Leishmania</i> and it is a significant global health problem. The disease has a wide clinical spectrum, from tegumentary leishmaniasis (TL) that encompasses cutaneous (CL), mucosal (ML) and cutaneous-diffuse (CDL) forms, to the potentially fatal systemic visceral leishmaniasis (VL). Neurological manifestations are not generally considered as classical clinical signs or symptoms of leishmaniasis, but in this review, we present evidence that this is a false assumption. We examine brain involvement in human and canine leishmaniasis and the contribution of animal models for studying cerebral <i>Leishmania</i> infection. Clinical descriptions of brain involvement are presented, and evidence of <i>Leishmania</i> invasion of the central nervous system. Notably, evidence for brain involvement comes from considerable studies in the dog and covers aspects of disruption of the blood-brain and blood-cerebrospinal fluid barriers and the nature of the inflammatory response.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70209","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autophagy, Apoptosis, and Inflammatory Mechanisms in Chronic Respiratory Diseases: Interplay in Special Reference to Mitochondrial-ER Stress Axis","authors":"Aditi Chitale,&nbsp;Smriti Verma,&nbsp;Madhav Nilakanth Mugale","doi":"10.1002/cbf.70203","DOIUrl":"10.1002/cbf.70203","url":null,"abstract":"<div>\u0000 \u0000 <p>Chronic respiratory diseases (CRDs) such as asthma, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and lung cancer, along with other CRDs, continue to be a major cause of morbidity and mortality globally and constitute a growing global health burden. There is growing evidence that the etiology of these conditions is primarily driven by organelle stress, specifically mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Mitochondria, which are highly susceptible to environmental stressors such as hypoxia, pollution, and tobacco smoke, can fail, leading to epithelial cell apoptosis, metabolic dysregulation, fibrosis, excessive mitochondrial reactive oxygen species (mtROS), altered calcium signaling, and impaired mitophagy. Similarly, unresolved ER stress triggers maladaptive unfolded protein response signaling, which in turn promotes epithelial damage, mucus hypersecretion, fibroblast activation, and tumor growth. Through ROS signaling and calcium flux, crosstalk between the mitochondria and the ER amplifies these maladaptive pathways. Dysregulated autophagy can promote tissue remodeling, inflammation, and tumor survival when it is either impaired or excessive. Another layer is added by apoptosis, which upsets tissue homeostasis by excessive fibroblast survival or epithelial cell death. Chronic inflammation is fueled by immune dysregulation and perpetual organelle stress, which exacerbates disease progression and resistance to therapy. Promising treatment options include adenosine monophosphate-activated protein kinase - mammalian target of rapamycin <b>(</b>AMPK–mTOR) regulators, ER stress modulators, mitochondrial-targeted antioxidants, and immunometabolic therapies that target organelle stress pathways. This review summarizes current insights into organelle stress responses in CRDs, with a focus on their integration with autophagy, apoptosis, and inflammation, and highlights the future approaches for precision medicine therapies aimed at alleviating disease burden.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JOSD1 Deubiquitinates Twist1 and Facilitates Epithelial–Mesenchymal Transition in Glioblastoma","authors":"Jiaquan Song,&nbsp;Wenjin Qiu,&nbsp;Ruting Wei,&nbsp;Wu Cen,&nbsp;Xiaotong Yang,&nbsp;Daijun Shen,&nbsp;Tangfeng Zhang,&nbsp;Yimin Chen,&nbsp;Shibin Song","doi":"10.1002/cbf.70208","DOIUrl":"10.1002/cbf.70208","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioblastoma (GBM) is a lethal brain tumor where diffuse invasion and a mesenchymal phenotype drive therapy resistance. Maintaining proteostasis through ubiquitin editing is a crucial stress-adaptive mechanism in cancer, but its role in GBM invasiveness is unclear. We analyzed JOSD1 expression in clinical samples and assessed its correlation with patient survival. Gain- and loss-of-function studies in GBM cell lines were performed to evaluate the role of JOSD1 in invasion, migration, proliferation, and the regulation of epithelial-to-mesenchymal transition (EMT) markers. Protein-protein interaction, deubiquitination, and cycloheximide chase assays were used to define the mechanistic relationship between JOSD1 and Twist1. Rescue experiments with Twist1 re-expression were conducted to confirm the functional axis. JOSD1 was markedly upregulated in GBM and high expression correlated with poor patient survival. JOSD1 overexpression promoted invasion, migration, proliferation, and an EMT-like shift (decreased E-cadherin, increased N-cadherin and Vimentin), while its silencing had opposite effects. Mechanistically, JOSD1 directly bound to and deubiquitinated Twist1, preventing its proteasomal degradation and extending its protein half-life. JOSD1 depletion accelerated Twist1 turnover, and re-expression of Twist1 rescued the impaired invasiveness and growth in JOSD1-deficient cells. Conversely, Twist1 knockdown abrogated the pro-invasive effects of JOSD1 overexpression. Our findings define a JOSD1–Twist1 axis that sustains a mesenchymal, invasive phenotype in GBM by regulating Twist1 protein stability. This links ubiquitin-dependent proteostasis to GBM pathogenicity, suggesting that targeting JOSD1 may represent a therapeutic strategy for aggressive, mesenchymal GBM. Glioblastoma remains one of the most lethal human cancers, and effective strategies to block its diffuse invasion are urgently needed. Here we identify the deubiquitinase JOSD1 as a previously unrecognized driver of epithelial–mesenchymal transition and invasion in glioblastoma. JOSD1 directly binds and deubiquitinates the transcription factor Twist1, preventing its proteasomal degradation and sustaining a mesenchymal, highly motile phenotype. Genetic depletion inhibition of JOSD1 destabilizes Twist1, suppresses invasion, and attenuates tumor growth in preclinical models. Clinically, JOSD1 is markedly upregulated in glioma tissues and its high expression predicts poor patient survival. Our findings nominate the JOSD1–Twist1 axis as a druggable vulnerability for invasive glioblastoma and support future development of JOSD1-targeted therapies.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA H19: A Potential Diagnostic and Therapeutic Target for Kidney Diseases","authors":"Hamza Malik Okuyan,&nbsp;Ayça Coskun,&nbsp;Şeyda Öznur Ayçiçek Özen,&nbsp;Mehmet A. Begen,&nbsp;Faruk Hilmi Turgut","doi":"10.1002/cbf.70210","DOIUrl":"10.1002/cbf.70210","url":null,"abstract":"<div>\u0000 \u0000 <p>Kidney diseases (KDs) impact over 800 million individuals globally, leading to significant morbidity and mortality. KDs place significant socioeconomic burdens on healthcare systems and lower patients' quality of life. Recent advancements and persuasive evidence on RNA biology have highlighted that the lncRNA world is a promising field for elucidating molecular mechanisms of kidney diseases and identifying novel diagnostic markers and therapeutic targets. Recent studies have highlighted that lncRNA H19, the first-reported transcript, plays a critical role in a variety of kidney diseases and, therefore, merits further investigation. Here, we focus on what is currently known about the possible roles of lncRNA H19 in the molecular pathogenesis of KDs and discuss the current evidence regarding the diagnostic and therapeutic role of lncRNA H19 in the prevention and treatment of kidney diseases. Emerging evidence has suggested that lncRNA H19 may play a crucial role in the onset and progression of KDs by modulating a variety of cellular mechanisms, such as apoptosis, autophagy, inflammation, fibrosis, oxidative damage, proliferation, differentiation, and metastasis. Furthermore, lncRNA H19 shows promise as a therapeutic target and diagnostic marker for the management of KDs, providing new insights into the combat of this severe complication of KDs. Although most available evidence originates from preclinical and experimental models, growing findings suggest that lncRNA H19 possesses substantial translational potential as a diagnostic biomarker and therapeutic target, warranting validation in large-scale clinical cohorts.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High Glucose Triggers Macrophage Senescence Through Mitochondrial Dysfunction and Mitophagy Impairment","authors":"Liying Tang,&nbsp;Xiuting Huang,&nbsp;Pei Li","doi":"10.1002/cbf.70211","DOIUrl":"10.1002/cbf.70211","url":null,"abstract":"<div>\u0000 \u0000 <p>Chronic hyperglycemia accelerates immune aging and contributes to diabetic complications, yet the mitochondrial mechanisms responsible for macrophage senescence remain unclear. In this study, both cultured and primary macrophages were treated with high glucose to model hyperglycemic conditions. High glucose significantly increased markers of macrophage senescence, including SA-β-Gal staining, expression of p16 and p21, and secretion of pro-inflammatory cytokines. Mitochondrial dysfunction was evident, as shown by loss of mitochondrial membrane potential (ΔΨm) and elevated mitochondrial reactive oxygen species (mtROS). In addition, mitophagy was impaired, with PINK1 accumulation and reduced Parkin recruitment. Rescue experiments demonstrated that treatment with the mitochondria-targeted antioxidant MitoTempo, the general antioxidant N-acetylcysteine, or the anti-diabetic drug metformin effectively restored mitochondrial function and alleviated senescence. These findings indicate that mitochondrial dysfunction and impaired mitophagy are central to high glucose-induced macrophage senescence, and that targeting mitochondrial oxidative stress with antioxidants or metformin may offer a promising strategy to mitigate immune aging and inflammation associated with metabolic disorders.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147637980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"d-Pinitol Rescues Osteoblast Differentiation From Tumor Necrosis Factor-Alpha-Mediated Suppression via β-Galactoside α-2,6-Sialyltransferase 1 Induction","authors":"Kyeong-Min Kim,&nbsp;Su-Jeong Kim,&nbsp;Won-Gu Jang","doi":"10.1002/cbf.70213","DOIUrl":"10.1002/cbf.70213","url":null,"abstract":"<div>\u0000 \u0000 <p><span>d</span>-pinitol, a naturally occurring inositol derivative found in legumes and soy-based foods, has shown various biological effects, including anti-inflammatory and insulin-sensitizing activities. However, its role in osteoblast differentiation under inflammatory conditions remains unclear. In this study, we investigated whether <span>d</span>-pinitol alleviates tumor necrosis factor-alpha (TNF-α)-induced suppression of osteogenic gene expression in MC3T3-E1 pre-osteoblasts. Using RT-PCR, real-time PCR, and Western blot analyses, we found that <span>d</span>-pinitol significantly restored the expression of osteogenic markers inhibited by TNF-α. Mechanistically, <span>d</span>-pinitol treatment markedly suppressed TNF-α-mediated upregulation of CREBH and Smurf1, negative regulators of osteoblast differentiation. Importantly, <span>d</span>-pinitol strongly induced the expression of β-galactoside α-2,6-sialyltransferase 1 (ST6Gal-1), and overexpression of ST6Gal-1 alone also decreased CREBH and Smurf1 expression. Furthermore, both <span>d</span>-pinitol and ST6Gal-1 overexpression attenuated TNF-α-induced endoplasmic reticulum (ER) stress markers, including ATF4, ATF6, EDEM, and BiP. These findings collectively suggest that <span>d</span>-pinitol promotes osteoblast differentiation under inflammatory stress by inducing ST6Gal-1 expression, thereby suppressing the CREBH–Smurf1 signaling axis and ER stress pathways. Our results highlight the potential therapeutic implications of <span>d</span>-pinitol in managing inflammatory bone diseases.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147637988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding P21 Activated Kinase-1 (PAK1) and Drug-Resistance Enigma","authors":"Sambuddha Sengupta,&nbsp;Ganesh Venkatraman","doi":"10.1002/cbf.70202","DOIUrl":"10.1002/cbf.70202","url":null,"abstract":"<div>\u0000 \u0000 <p>Drug resistance, also known as chemoresistance, is a known impediment in fighting cancers. Pak1 (p21-activated kinase), a serine/threonine kinase, is a known oncogene implicated in tumor progression and associated with poor prognosis in cancer patients. Pak1 has been reported to be mechanistically contributing to drug resistance to tamoxifen and gemcitabine. Using an integrative approach, the present study investigated Pak1 and its precise role in conferring chemoresistance alongside other known kinases. Study identified 25 additional kinases contributing to resistance to 12 commonly used drugs in clinics for the treatment of breast, head and neck, and pancreatic cancers. The study analysis revealed that mutated Pak1 and more than one kinase were likely to be involved in drug resistance in patients associated with poor prognosis. The study concluded that the detection of altered kinases in resistant tumors is imperative, and a combination of kinase inhibitors could be useful for treatment rather than single agents to improve treatment outcomes.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Sodium and Gut Klebsiella Are Positively Related to Osteoporosis","authors":"Xiuhong Cao,&nbsp;Pengbing Hua,&nbsp;Yongjun Zhu,&nbsp;Hongwang Cui,&nbsp;Fabiao Yu,&nbsp;Tongmeng Jiang","doi":"10.1002/cbf.70207","DOIUrl":"10.1002/cbf.70207","url":null,"abstract":"<div>\u0000 \u0000 <p>Emerging evidence suggests a link between gut microbiota dysbiosis and osteoporosis. However, specific bacterial taxa and metabolic correlates in human osteoporosis remain poorly characterized. This study explored gut microbial profiles and serum biochemical markers in osteoporosis patients compared to non-osteoporosis individuals in Hainan, China. Fecal samples and serum biochemistry, including liver function, kidney function, lipid profiles, and ion concentrations, were analyzed in six osteoporosis patients and six non-osteoporosis individuals. Gut microbiota composition was assessed via 16S rDNA gene sequencing. Differential abundance analysis and linear discriminant analysis effect size (LEfSe) were performed to identify biomarkers. Osteoporosis patients exhibited significantly higher serum sodium levels (143.31 ± 1.40 mmol/L vs. 140.00 ± 2.60 mmol/L, <i>p</i> &lt; 0.05) and reduced HDL cholesterol (1.03 ± 0.14 vs. 1.33 ± 0.09 mmol/L, <i>p</i> &lt; 0.05). Microbiota profiling revealed 11 enriched and seven depleted bacteria in patients by LEfSe analysis. Notably, <i>Klebsiella</i> showed the highest relative abundance increase in osteoporosis patients, while <i>Megamonas</i> abundance was significantly reduced as indicated by square root of the indicator value (sqrtIVt). This pilot study identifies elevated serum sodium and gut <i>Klebsiella</i> enrichment as potential metabolic and microbial signatures of osteoporosis in the Hainan population. These findings suggest that modulation of gut microbiota and sodium management could be explored as preventive strategies. Larger, multiethnic cohorts and mechanistic studies are needed to validate these biomarkers and elucidate causality.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Inflammatory Effect of miR-197-3p-Loaded Microvesicles in Familial Mediterranean Fever Mouse Model","authors":"Yeliz Z. Akkaya-Ulum,&nbsp;Emre Nalbant,&nbsp;Baris Ulum,&nbsp;Tayfun Hilmi Akbaba,&nbsp;Jae Jin Chae,&nbsp;Banu Balci-Peynircioglu","doi":"10.1002/cbf.70205","DOIUrl":"10.1002/cbf.70205","url":null,"abstract":"<div>\u0000 \u0000 <p>Familial Mediterranean Fever (FMF) is an inherited autoinflammatory disease triggered by Mediterranean Fever (MEFV) gene mutations that lead to spontaneous pyrin inflammasome activation and exaggerated pro-inflammatory cytokine secretion. The V726A knock-in (KI) mouse model of FMF mimics most of the clinical and immunologic manifestations of the disease, such as recurrent febrile attacks and systemic inflammation. Here, we explored the proof-of-concept evaluation of miR-197-3p-loaded microvesicles (MVs) as a therapeutic approach in the FMF KI mouse model. MVs were purified and structurally characterized through Cryo-Transmission Electron Microscopy (Cryo-TEM), establishing their integrity and size (100–1000 nm), which are compatible for nucleic acid delivery. The miR-197-3p-loaded MVs were retro-orbitally injected in FMF KI mice, and the outcomes were investigated in terms of interleukin-1beta (IL-1β) secretion, CD11b expression in total blood, spleen weight (mg) and back length as a morphological feature. miR-197-3p-loaded MV treatment in <i>Mefv</i>^V726A/V726A mouse model of FMF decreased the IL-1β level and the expression of CD11b and improved clinical inflammation manifestations. The results show that miR-197-3p-loaded MVs modulate inflammation, as well as improve phenotypic features of FMF, which is a promising, cell-free potential therapeutic strategy for autoinflammatory diseases. This study represents a preliminary proof-of-concept evaluation of miR-197-3p-loaded microvesicles in a murine FMF model, and further long-term and large-scale studies are required before clinical translation can be considered.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isolation and Identification of Bacillus velezensis G52 and Its Growth-Promoting Mechanism on Navel Orange Seedlings.","authors":"Wenyuan Zhao, Tao Peng, Haojie Cao, Huimin Huang, Ruiqi Liu, Shuijing Yu","doi":"10.1002/cbf.70222","DOIUrl":"https://doi.org/10.1002/cbf.70222","url":null,"abstract":"<p><p>This study isolated and screened a multifunctional plant-growth-promoting bacterium, Bacillus sp. G52, from the rhizosphere soil of Gannan navel oranges. Through pot experiments and genomic analysis, the growth-promoting effects and molecular mechanisms of strain G52 on navel orange seedlings were systematically evaluated. The results showed that strain G52 could secrete indole-3-acetic acid (IAA, yield: 18.68 ± 0.81 mg/L), siderophores (yield: 47.10 ± 1.03%), and phosphate-solubilizing substances (91.85 ± 4.94 mg/L) while also exhibiting ACC deaminase activity and ammonia production. Pot experiments demonstrated that inoculation with G52 significantly increased seedling height (12.51%), stem diameter (10.97%), biomass (27.87% in shoots, 41.13% in roots), and chlorophyll content (37.40% increase in total chlorophyll). Additionally, G52-treated seedlings showed enhanced antioxidant enzyme activities (SOD, POD, CAT), indicating improved stress resistance. Genomic analysis revealed that G52 carries functional genes related to IAA synthesis (e.g., trpA-trpF) and siderophore production (e.g., ent gene cluster), further confirming the molecular basis of its growth-promoting potential. Phylogenetic analysis indicated a 99.7% similarity between G52 and Bacillus velezensis. This study provides a theoretical foundation for developing multifunctional Bacillus-based biofertilizers, contributing to sustainable agricultural development.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"44 4","pages":"e70222"},"PeriodicalIF":2.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}