Biochemistry and Biophysics Reports最新文献

{"title":"Oxidative stress-induced NCC activation in the development of nocturnal polyuria in mice: Therapeutic potential of a sustained hydrogen-releasing silicon-based agent","authors":"Yosuke Sekii ,&nbsp;Hiroshi Kiuchi ,&nbsp;Kentaro Takezawa ,&nbsp;Norichika Ueda ,&nbsp;Takahiro Imanaka ,&nbsp;Sohei Kuribayashi ,&nbsp;Koichi Okada ,&nbsp;Shinichiro Fukuhara ,&nbsp;Ryoichi Imamura ,&nbsp;Hiromistu Negoro ,&nbsp;Yuki Kobayashi ,&nbsp;Hikaru Kobayashi ,&nbsp;Norio Nonomura","doi":"10.1016/j.bbrep.2025.101923","DOIUrl":"10.1016/j.bbrep.2025.101923","url":null,"abstract":"<div><div>Nocturnal polyuria is a prevalent condition associated with significant deterioration in quality of life and increased risk of mortality. Despite its clinical relevance, the underlying pathogenesis is poorly understood, and existing therapies have limited efficacy. A recent study in mouse model revealed that overactivation of the intrarenal SPAK (STE20/SPS1-related proline–alanine rich protein kinase)–sodium chloride co-transporter (NCC) pathway in the distal renal tubule is a crucial mechanism contributing to nocturnal polyuria. Here, we demonstrate that increased oxidative stress in the kidney activates the NCC, leading to insufficient sodium excretion during the active period and compensatory sodium excretion during the inactive period, resulting in polyuria during the inactive period. In addition, we show that a newly developed antioxidant—a silicon component agent—reduced oxidative stress and inhibited NCC activation, resulting in the amelioration of polyuria during the inactive period. These findings highlight the critical contributions of intrarenal oxidative stress to the pathogenesis of nocturnal polyuria and suggest that silicon-based agent holds promise for clinical application as a novel treatment for nocturnal polyuria.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101923"},"PeriodicalIF":2.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative analysis of RNA-Seq data and machine learning approaches to identify Biomarkers for Rhizoctonia solani resistance in sugar beet","authors":"Bahman Panahi ,&nbsp;Mahdi Hassani ,&nbsp;Nahid Hosseinzaeh Gharajeh","doi":"10.1016/j.bbrep.2025.101920","DOIUrl":"10.1016/j.bbrep.2025.101920","url":null,"abstract":"<div><div>Rhizoctonia solani is a significant pathogen that causes crown and root rot in sugar beet (Beta vulgaris), leading to considerable yield losses. To develop resilient cultivars, it is crucial to understand the molecular mechanisms underlying both resistance and susceptibility. In this study, we employed RNA-Seq analysis alongside machine learning techniques to identify key biomarkers associated with resistance to R. solani. We ranked differentially expressed genes (DEGs) using feature-weighting algorithms, such as Relief and kernel-based methods, to model expression patterns between sensitive and tolerant cultivars. Our integrative approach identified several candidate genes, including Bv5g001004 (encoding Ethylene-responsive transcription factor 1A), Bv8g000842 (encoding 5′-adenylylsulfate reductase 1), and Bv7g000949 (encoding Heavy metal-associated isoprenylated plant protein 5). These genes are involved in stress signal transduction, sulfur metabolism, and disease resistance pathways. Graphical visualizations of the Random Forest and Decision Tree models illustrated the decision-making processes and gene interactions, enhancing our understanding of the complex relationships between sensitive and tolerant genotypes. This study demonstrates the effectiveness of integrating RNA-Seq and machine learning techniques for biomarker discovery and highlights potential targets for developing R. solani-resistant sugar beet cultivars. The findings provide a robust framework for improving crop enhancement strategies and contribute to sustainable agricultural practices by increasing stress resilience in economically important crops.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101920"},"PeriodicalIF":2.3,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic HSD17B6 is dispensable for diet-induced fatty liver disease in mice","authors":"Delong Yuan ,&nbsp;Nan Bai ,&nbsp;Qihan Zhu ,&nbsp;Shaoxuan Song ,&nbsp;Anyuan He ,&nbsp;Jianqing Wang ,&nbsp;Yali Chen","doi":"10.1016/j.bbrep.2025.101924","DOIUrl":"10.1016/j.bbrep.2025.101924","url":null,"abstract":"<div><div>Metabolic dysfunction-associated fatty liver disease (MAFLD) affects up to a third of the global population, which causes huge both clinical and economic burdens. However, its therapeutic strategy is still limited. Steroid dysregulation plays a pivotal role in the homeostasis of lipid metabolism. 17-beta-hydroxysteroid dehydrogenase type 6 (HSD17B6)—one member of 17β-HSDs, encoded by the gene <em>Hsd17b6</em>, catalyzes the synthesis of androsterone and estrone—steroid hormones. However, whether the manipulation of HSD17B6 could ameliorate diet-induced fatty liver disease remains unknown. Here, we found that the expression of <em>Hsd17b6</em> is enriched in the liver in both humans and mice. The data of single-cell RNA-seq suggests that <em>Hsd17b6</em> appears to be exclusively expressed in hepatocytes—the parenchymal cells of the liver. Furthermore, the hepatic expression of <em>Hsd17b6</em> is correlated with fatty liver disease. A mouse model with <em>Hsd17b6</em> deletion in the liver (HLKO) is successfully generated via the administration of AAV8 expressing Cre recombinase (driven by TBG—a liver-specific promoter) and sgRNAs of <em>Hsd17b6</em> to Cre-dependent Cas9 mice. Control and HLKO mice were challenged with the high-fat choline-deficient diet—a diet widely used for the model generation of fatty liver disease. Interestingly, the HLKO liver shows a special proteome signature, with the altered proteins enriched in the Golgi apparatus. However, the deletion of <em>Hsd17b6</em> does not affect fatty liver disease in terms of fat accumulation, inflammation, and hepatic fibrosis. Taken together, our study suggests that the expression of <em>Hsd17b6</em> is enriched in the liver and correlated with fatty liver disease but its hepatic deletion does not affect diet-induced fatty liver disease.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101924"},"PeriodicalIF":2.3,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell RNA sequencing provides new insights into the interaction between astrocytes and neurons after spinal cord injury in mice","authors":"Zhi Tang ,&nbsp;Hengyang Lu ,&nbsp;Xiao Yang ,&nbsp;Mao Wu ,&nbsp;Junfeng Yang ,&nbsp;Shaoshuo Li ,&nbsp;Heng Liu ,&nbsp;Junkang Zhou ,&nbsp;Bin Tang ,&nbsp;Xinyao Du ,&nbsp;Fei Xu ,&nbsp;Yang Shao ,&nbsp;Jianwei Wang","doi":"10.1016/j.bbrep.2025.101917","DOIUrl":"10.1016/j.bbrep.2025.101917","url":null,"abstract":"<div><h3>Background</h3><div>Spinal cord injury (SCI) is a devastating neurological disease in which astrocytes play a central role. Understanding the relationship between different subtypes of astrocytes and neuron subtypes during the progression of SCI is critical to understanding the disease.</div></div><div><h3>Methods and results</h3><div>In this study, single-cell RNA sequencing (scRNA-seq) was used to analyze the transcriptome data of acute, subacute and intermediate stages of SCI in mice as well as normal tissues. Different subtypes of astrocytes and neuronal cells were identified and their dynamic changes and functionalities during the development of SCI. An intriguing discovery was the identification of a specific subtype of astrocytes characterized by unique expression of Gap43, Vim, Aldoc, and Mt1. This subtype of cells shows similarities in gene expression with neurons and potentially transitioned into neurons during the course of SCI. Furthermore, we have uncovered the important role of the glycolytic pathway in this cellular transformation process. Furthermore, through cellular interaction analysis, we validated pathways (mdk-ptprz1,ptn-ptprz1,ptn-sdc3) associated with the potential conversion of these specific cell subsets into neurons. Finally, these cells were observed by fluorescence microscopy and critical gene expressions were validated by Western blot.</div></div><div><h3>Conclusions</h3><div>The results of this study not only deepen our understanding of the mechanisms underlying SCI, but also provide new insights and opportunities for the development of novel therapeutic strategies and interventions.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101917"},"PeriodicalIF":2.3,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistance to FLT3 inhibitors involves different molecular mechanisms and reduces new DNA synthesis","authors":"Jingmei Yang,&nbsp;Ran Friedman","doi":"10.1016/j.bbrep.2024.101894","DOIUrl":"10.1016/j.bbrep.2024.101894","url":null,"abstract":"<div><div>Acute myeloid leukaemia (AML) is a hard to treat blood cancer. Mutations in FLT3 are common among the genetic aberrations that characterise the cancer. Patients initially react to FLT3 inhibitors but drug resistance is a hinder to successful therapy. To better understand the mechanisms leading to drug resistance, we generated four AML cell lines resistant to the inhibitors gilteritinib or FF-10101, and explored their resistance mechanisms. We further tested whether the novel inhibitor Chen-9u could be used to limit cell growth. The results showed that each of the four resistant cell lines became resistant through a different mechanism. Resistant cells showed decreased FLT3 and increased NRAS pathway activity and reduced DNA synthesis due to decrease in CDK4 activity. Resistance mechanisms included resistance mutations in FLT3 (C695F and N701K), and a novel mutation in NRAS (G12C). In a fourth line, resistance might have developed through a MYCN mutation. Cell growth was inhibited by Chen-9u and resistant clones could not be obtained with this inhibitor. The results highlight opportunities and limitations. On the one hand, resistant cells were produced due to different mechanisms, showing the versatility of tumour cells. Furthermore, resistance developed to the most advanced inhibitors, one of which is covalent and the other non-covalent but highly specific. On the other hand, it is shown that DNA synthesis is reduced, which means that resistance has evolutionary consequences. Finally, the novel drug-resistant cell lines may serve as useful models for better understanding of the cellular events associated with inherent and acquired drug resistance.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101894"},"PeriodicalIF":2.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Screening of biomarkers for diagnosing chronic kidney disease and heart failure with preserved ejection fraction through bioinformatics analysis","authors":"Can Hou ,&nbsp;Jiayi Xu ,&nbsp;Min Zhou ,&nbsp;Junyu Huo ,&nbsp;Xiaofei Wang ,&nbsp;Wanying Jiang ,&nbsp;Tong Su ,&nbsp;Hui Wang ,&nbsp;Fang Jia","doi":"10.1016/j.bbrep.2024.101911","DOIUrl":"10.1016/j.bbrep.2024.101911","url":null,"abstract":"<div><h3>Background</h3><div>Previous research has established that chronic kidney disease (CKD) and heart failure with preserved ejection fraction (HFpEF) often coexist. Although we have a preliminary understanding of the potential correlation between HFpEF and CKD, the underlying pathophysiological mechanisms remain unclear. This study aimed to elucidate the molecular mechanisms associated with CKD and HFpEF through bioinformatics analysis.</div></div><div><h3>Methods</h3><div>Datasets for HFpEF and CKD were obtained from the Gene Expression Omnibus (GEO) database. The R software package “limma” was employed to conduct differential expression analysis. Functional annotation was performed using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). We conducted weighted gene co-expression network analysis (WGCNA), correlation analysis with autophagy, ferroptosis, and immune-related processes, as well as transcriptional regulation analysis, immune infiltration analysis, and diagnostic performance evaluation. Finally, the diagnostic potential of the identified hub genes for CKD and HFpEF was assessed using ROC curve analysis (GSE37171).</div></div><div><h3>Results</h3><div>Differential expression analysis revealed 58 overlapping genes, comprised of 40 up-regulated and 18 down-regulated genes. Both GO and KEGG analyses indicated enriched pathways relevant to both disorders. WGCNA identified 4086 genes associated with CKD. Further comparison with differentially expressed genes (DEGs) identified three hub genes (KLF4, SCD, and SEL1L3) that were linked to autophagy, ferroptosis, and immune processes in both conditions. Additionally, a miRNA-mRNA regulatory network involving 376 miRNAs and 12 transcription factors (TFs) was constructed. ROC curve analysis was performed to evaluate the diagnostic utility of the hub genes for CKD and HFpEF.</div></div><div><h3>Conclusion</h3><div>This study elucidated shared pathogenic mechanisms and identified diagnostic markers common to both HFpEF and CKD. The identified hub genes show promise as potential tools for early diagnosis and treatment strategies for these conditions.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101911"},"PeriodicalIF":2.3,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143057888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electric-field induced sleep promotion and lifespan extension in Gaucher's disease model flies","authors":"Takaki Nedachi ,&nbsp;Haruhisa Kawasaki ,&nbsp;Eiji Inoue ,&nbsp;Takahiro Suzuki ,&nbsp;Yuzo Nakagawa-Yagi ,&nbsp;Norio Ishida","doi":"10.1016/j.bbrep.2025.101915","DOIUrl":"10.1016/j.bbrep.2025.101915","url":null,"abstract":"<div><div>Gaucher's disease (GD) is a genetic disease characterized by a mutation in the metabolic enzyme glucocerebrosidase (GBA1), leading to the accumulation of glucosylceramide in tissues. We previously discovered that a <em>minos</em>-inserted mutation in the <em>GBA1</em> gene of fruit flies, <em>Drosophila melanogaster</em>, mimics human neuronopathic GD (nGD) characteristics, providing a promising model for studying the molecular mechanisms of the disease. We also reported that extremely low-frequency electric fields (ELF-EFs) promote sleep and extend the lifespan of wild-type flies.</div><div>In this study, we show that ELF-EFs have health-promoting effects on nGD model flies.</div><div>Firstly, the total sleep time and sleep episode duration of EF-exposed nGD model flies increased. EFs also extended the lifespans of nGD model flies. Additionally, the expression of the endoplasmic reticulum stress-related gene <em>PERK</em> and autophagy-related gene <em>p62</em> were elevated after EF exposure. The effects of EF exposure on nGD flies are associated with the change of these genes expression. Our findings suggest that EF exposure may be effective as an additional therapy for nGD.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101915"},"PeriodicalIF":2.3,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of novel microRNAs: Biomarkers for pathogenesis of hepatocellular carcinoma in mice model","authors":"Shivani Priya ,&nbsp;Lakhon Kma","doi":"10.1016/j.bbrep.2024.101896","DOIUrl":"10.1016/j.bbrep.2024.101896","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is the most fatal cancer that has affected both male and female populations globally. With poor diagnosis and patient survival rates, it has become a global need for scientists to come to the aid. The main objective of the study was to profile the miRNAs in the serum of Control and DEN-treated mice at different time intervals (4 Weeks, 8 Weeks, 12 Weeks, and 16 Weeks) and identify HCC-associated miRNA as putative early biomarkers along with the miRNA regulated candidate gene which may be involved in HCC. Our study group involves 4,8,12, &amp; 16 weeks 16-week-old treated male mice. Each group was sacrificed and analyzed for the stages of HCC. We employed <em>in silico</em> techniques for the small RNA-Seq and bioinformatics pipeline for further analysis. Our analysis revealed over 400 differentially expressed miRNAs in each treated sample and 10 novel miRNAs. The downstream analysis of these differentially expressed miRNAs, and their target genes opened an arena of different biological processes and pathways that these miRNAs affect during the development of HCC. The work has a promising role as the miRNAs predicted through this study can be used as biomarkers for early detection of HCC.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101896"},"PeriodicalIF":2.3,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive outline of the role of non-coding RNAs in vitiligo","authors":"Fateme Sadat Feghahati,&nbsp;Soudeh Ghafouri-Fard","doi":"10.1016/j.bbrep.2025.101916","DOIUrl":"10.1016/j.bbrep.2025.101916","url":null,"abstract":"<div><div>Vitiligo is a common skin depigmentation condition caused by selective destruction of melanocytes. It is regarded as a polygenic disorder. In addition to protein-coding loci, non-coding regions of the genome contribute to the pathogenesis of vitiligo. A bulk of evidence highlights contribution of different classes of non-coding RNAs in this condition. Expression profile of different non-coding RNAs has been evaluated in the plasma, serum, blood cells and skin samples of patients with vitiligo. Notably, these transcripts not only partake the pathogenesis of vitiligo, but also are regarded as putative targets for prospective treatment strategies for this disorder. The current review focuses on depicting the role of miRNAs, long non-coding RNAs and circular RNAs in the etiology of vitiligo. Moreover, we discuss the shared functions of these transcripts in the pathogenesis of vitiligo and melanoma.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101916"},"PeriodicalIF":2.3,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methylmalonic acid at the serum level in the elderly contributes to cell growth via mitochondrial dysfunction in colorectal cancer cell spheroids","authors":"Arowu R. Tanaka,&nbsp;Chiho Murakami,&nbsp;Hideya Yamamoto","doi":"10.1016/j.bbrep.2024.101909","DOIUrl":"10.1016/j.bbrep.2024.101909","url":null,"abstract":"<div><div>Methylmalonic acid (MMA) is a small molecule produced during the metabolism of propionate and branched-chain amino acids. Recently, it has been reported that the blood concentration of MMA increases with age and promotes lung cancer metastasis. However, little is known regarding its effects on cancers other than lung cancer. In the present study, we examined the effects of MMA on colorectal cancer cell spheroids. We found that MMA promoted the proliferation of colorectal cancer spheroids at physiological concentrations that can be exhibited by the elderly and induced mitochondrial reactive oxygen species generation, which in turn affected the promotion of cell growth. MMA treatment also induces a metabolic shift in the glycolytic system. These results suggest that MMA may promote cancer cell proliferation by decreasing mitochondrial function, inducing a metabolic shift, and provide new insights into the effects of aging on cancer.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101909"},"PeriodicalIF":2.3,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11780164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}