Molecular and Cellular Biochemistry最新文献

{"title":"MicroRNA signatures in osteosarcoma: diagnostic insights and therapeutic prospects.","authors":"Mritunjoy Dey, Palina Skipar, Ewa Bartnik, Jakub Piątkowski, Dorota Sulejczak, Anna M Czarnecka","doi":"10.1007/s11010-024-05135-5","DOIUrl":"10.1007/s11010-024-05135-5","url":null,"abstract":"<p><p>Osteosarcoma (OSa) is the most prevalent primary malignant bone tumor in children and adolescents, characterized by complex genetic and epigenetic alterations. Traditional treatments face significant challenges due to high rates of drug resistance and lack of targeted therapies. Recent advances in microRNA (miRNA) research have opened new avenues for understanding and treating osteosarcoma. This review explores the many critical functions of miRNAs in osteosarcoma, particularly their potential for clinical use. The review highlights two key areas where miRNAs could be beneficial. Firstly, miRNAs can act as biomarkers for diagnosing osteosarcoma and predicting patient prognosis. Secondly, specific miRNAs can regulate cellular processes like proliferation, cell death, migration, and even resistance to chemotherapy drugs in osteosarcoma. This ability to target multiple pathways within cancer cells makes miRNA-based therapies highly promising. Additionally, though the interaction between miRNAs and circular RNAs (circRNAs) falls outside the scope of the paper, it has also been discussed briefly. While miRNA-based therapies offer exciting possibilities for targeting multiple pathways in osteosarcoma, challenges remain. Efficient delivery, potential off-target effects, tumor complexity, and rigorous testing are hurdles to overcome before these therapies can reach patients. Despite these challenges, continued research and collaboration among scientists, clinicians, and regulatory bodies hold the promise of overcoming them. This collaborative effort can pave the way for the development of safe and effective miRNA-based treatments for osteosarcoma.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2065-2075"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NBS1 dePARylation by NUDT16 is critical for DNA double-strand break repair.","authors":"Zhen Zhang, William E Samsa, Zihua Gong","doi":"10.1007/s11010-024-05140-8","DOIUrl":"10.1007/s11010-024-05140-8","url":null,"abstract":"<p><p>NBS1, a protein linked to the autosomal recessive disorder Nijmegen breakage syndrome, plays an essential role in the DNA damage response and DNA repair. Despite its importance, the mechanisms regulating NBS1 and the impact of this regulation on DNA repair processes remain obscure. In this study, we discovered a new post-translational modification of NBS1, ADP-ribosylation. This modification can be removed by the NUDT16 hydrolase. The loss of NUDT16 results in a reduction of NBS1 protein levels due to NBS1 PARylation-dependent ubiquitination and degradation, which is mediated by the PAR-binding E3 ubiquitin ligase, RNF146. Importantly, ADP-ribosylation of NBS1 is crucial for its localization at DSBs and its involvement in homologous recombination (HR) repair. Additionally, the NUDT16-NBS1 interaction is regulated in response to DNA damage, providing further rationale for NBS1 regulation by NUDT16 hydrolase. In summary, our study unveils the critical role of NUDT16 in governing both the stability of NBS1 and recruitment of NBS1 to DNA double-strand breaks, providing novel insights into the regulation of NBS1 in the HR repair pathway.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2595-2609"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting cardiac fibrosis with Chimeric Antigen Receptor-Engineered Cells.","authors":"Qinghang Zhang, Jinjie Dai, Tianbao Liu, Wutian Rao, Dan Li, Zhengying Gu, Lin Huang, Jiayi Wang, Xumin Hou","doi":"10.1007/s11010-024-05134-6","DOIUrl":"10.1007/s11010-024-05134-6","url":null,"abstract":"<p><p>Cardiac fibrosis poses a significant challenge in cardiovascular diseases due to its intricate pathogenesis, and there is currently no standardized and effective treatment approach. The fibrotic process entails the involvement of various cell types and molecular mechanisms, such as fibroblast activation and proliferation, increased collagen synthesis, and extracellular matrix rearrangement. Traditional therapies often fall short in efficacy or carry substantial side effects. However, recent studies have shown that Chimeric Antigen Receptor T (CAR-T) cells can selectively target and eliminate activated cardiac fibroblasts (CFs) in mice, leading to reduced cardiac fibrosis and improved myocardial tissue compliance. This breakthrough presents a new and promising avenue for treating cardiac fibrosis. Currently, CAR-T cell-based therapy for cardiac fibrosis is undergoing animal experimentation, indicating ample scope for enhancement. Future investigations could explore the application of CAR cell therapy in cardiac fibrosis treatment, including the potential of CAR-natural killer (CAR-NK) cells and CAR macrophages (CAR-M), offering novel insights and strategies for combating cardiac fibrosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"2103-2116"},"PeriodicalIF":3.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota and microRNAs as biomarkers in Parkinson's disease: early identification, diagnostic and potential treatments.","authors":"Javier Hernández-García, Patricia Muro-Reche, Esteban Orenes-Piñero","doi":"10.1007/s11010-025-05271-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05271-6","url":null,"abstract":"<p><p>The gut microbiota can affect both the enteric and the central nervous system, influencing individuals and their brain regulation. In this work, different pieces of scientific evidence are discussed, showing the relationship between changes in the microbiota and neurocognitive deterioration, focussing on Parkinson's disease (PD). Other factors that may cause or contribute to PD aetiology are the interactions between environmental factors and genetic susceptibility. According to the existing literature, there are several methods for the identification of neurocognitive impairment in different neurological diseases. However, such methods do not allow early identification, and therefore, the possibility of using other types of more effective diagnostic biomarkers in PD has also been investigated. Since this disease is characterised by specific microRNA (miRNA) expression, and the gut microbiota is an important factor in both PD and miRNA expression, the aim of this review is thoroughly analysing the role of microbiota and microRNAs in PD development. In addition, the relationship between these two factors and potential treatments will be also discussed.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dilated cardiomyopathy: from genes and molecules to potential treatments.","authors":"Xiumei Wang, Zekun Lang, Zeyi Yan, Jing Xu, Jinyuan Zhang, Lianhang Jiao, Haijun Zhang","doi":"10.1007/s11010-025-05269-0","DOIUrl":"https://doi.org/10.1007/s11010-025-05269-0","url":null,"abstract":"<p><p>Dilated cardiomyopathy is a myocardial condition marked by the enlargement of the heart's ventricular chambers and the gradual decline in systolic function, frequently resulting in congestive heart failure. Dilated cardiomyopathy has obvious familial characteristics, and mutations in related pathogenic genes can account for about 50% of patients with dilated cardiomyopathy. The most common genes related to dilated cardiomyopathy include TTN, LMNA, MYH7, etc. With more and more research on these genes, it will undoubtedly provide more potential targets and therapeutic pathways for the treatment of dilated cardiomyopathy. In addition, myocardial inflammation, myocardial metabolism abnormalities and cardiomyocyte apoptosis all have an important impact on the pathogenesis of dilated cardiomyopathy. Approximately half of sudden deaths among children and adolescents, along with the majority of patients undergoing heart transplantation, stem from cardiomyopathy. Therefore, precise and prompt clinical diagnosis holds paramount importance. Currently, diagnosis primarily hinges on the patient's medical background and imaging tests, with the significance of genetic testing steadily gaining prominence. The primary treatment for dilated cardiomyopathy remains heart transplantation. However, the scarcity of donors and the risk of severe immune rejection underscore the pressing need for novel therapies. Presently, research is actively exploring preclinical treatments like stem cell therapy as potential solutions.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis: a potential therapeutic target in cardio-cerebrovascular diseases.","authors":"Chenlong Jiang, Yang Yan, Tianlin Long, Jiawei Xu, Cuicui Chang, Meili Kang, Xuanqi Wang, Yuhua Chen, Junlin Qiu","doi":"10.1007/s11010-025-05262-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05262-7","url":null,"abstract":"<p><p>Cardio-cerebrovascular diseases (CCVDs) are the leading cause of global mortality, yet effective treatment options remain limited. Ferroptosis, a novel form of regulated cell death, has emerged as a critical player in various CCVDs, including atherosclerosis, myocardial infarction, ischemia-reperfusion injury, cardiomyopathy, and ischemic/hemorrhagic strokes. This review highlights the core mechanisms of ferroptosis, its pathological implications in CCVDs, and the therapeutic potential of targeting this process. Additionally, it explores the role of Chinese herbal medicines (CHMs) in mitigating ferroptosis, offering novel therapeutic strategies for CCVDs management. Ferroptosis is regulated by several key pathways. The GPX4-GSH-System Xc- axis is central to ferroptosis execution, involving GPX4 using GSH to neutralize lipid peroxides, with system Xc- being crucial for GSH synthesis. The NAD(P)H/FSP1/CoQ10 axis involves FSP1 regenerating CoQ10 via NAD(P)H, inhibiting lipid peroxidation independently of GPX4. Lipid peroxidation, driven by PUFAs and enzymes like ACSL4 and LPCAT3, and iron metabolism, regulated by proteins like TfR1 and ferritin, are also crucial for ferroptosis. Inhibiting ferroptosis shows promise in managing CCVDs. In atherosclerosis, ferroptosis inhibitors reduce iron accumulation and lipid peroxidation. In myocardial infarction, inhibitors protect cardiomyocytes by preserving GPX4 and SLC7A11 levels. In ischemia-reperfusion injury, targeting ferroptosis reduces myocardial and cerebral damage. In diabetic cardiomyopathy, Nrf2 activators alleviate oxidative stress and iron metabolism irregularities. CHMs offer natural compounds that mitigate ferroptosis. They possess antioxidant properties, chelate iron, and modulate signaling pathways like Nrf2 and AMPK. For example, Salvia miltiorrhiza and Astragalus membranaceus reduce oxidative stress, while some CHMs chelate iron, reducing its availability for ferroptosis. In conclusion, ferroptosis plays a pivotal role in CCVDs, and targeting it offers novel therapeutic avenues. CHMs show promise in reducing ferroptosis and improving patient outcomes. Future research should explore combination therapies and further elucidate the molecular interactions in ferroptosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peripheral nerves-cancer cross-talk: the next frontier in cancer treatment.","authors":"Leihan Wang, Teng Qi, Lingyun Tang, Yuehan Wang, Zhenni ChenLiu, Daorong Wang, Dong Tang","doi":"10.1007/s11010-025-05256-5","DOIUrl":"https://doi.org/10.1007/s11010-025-05256-5","url":null,"abstract":"<p><p>The nervous system, which regulates organogenesis, homeostasis, and plasticity of the organism during human growth and development, integrates physiological functions of all organ systems, including the immune system. Its extensive network of branches throughout the body reaches the tumor microenvironment (TME), where it secretes neurotransmitters that directly regulate or influence immune cells. This, in turn, indirectly affects the occurrence, development, and metastasis of cancer. Conversely, cancer cells are now understood to secrete neurotrophic factors that remodel the nervous system. Targeting the cross-talk between the nervous system and cancer represents a promising strategy for cancer treatment, some aspects of which have been confirmed in clinical trials. This review addresses gaps in our understanding of the interaction between peripheral nerves and various human cancers. At the intersection of neuroscience and cancer biology, new targets for neuroscience-based cancer therapies are emerging, establishing a significant new pillar in cancer treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Molecular and biochemical evidence on the protective role of ellagic acid and silybin against oxidative stress-induced cellular aging.","authors":"Maryam Baeeri, Solmaz Mohammadi-Nejad, Mahban Rahimifard, Mona Navaei-Nigjeh, Shermineh Moeini-Nodeh, Reza Khorasani, Mohammad Abdollahi","doi":"10.1007/s11010-025-05266-3","DOIUrl":"https://doi.org/10.1007/s11010-025-05266-3","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between herpesviruses and alzheimer's disease: a meta-analysis based on case-control studies.","authors":"Huilin Feng, Kexiao Pan, Zulfa Ismail Shabani, Hongju Wang, Wenqiang Wei","doi":"10.1007/s11010-025-05263-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05263-6","url":null,"abstract":"<p><p>Herpesviruses infection has been found to be implicated in the etiology of Alzheimer's disease (AD). However, the results remain controversial. This systematic meta-analysis was aimed to evaluate the relationship between Herpesviruses infection and the risk of developing AD. Relevant literature was searched from five databases, including CNKI, PubMed, Web of Science, Embase, and Cochrane Library, to obtain case-control studies (published between the date of database establishment and February 2025; no language restrictions) that compared the Herpesviruses positivity in AD patients and healthy controls. Among all existing studies, there are more abundant published case-control studies on the relationship between HSV-1, HCMV and Alzheimer's disease. Therefore, we chose these two viruses to further explore their association with Alzheimer's disease. The quality of the included studies was evaluated by the NOS scale. The Review Manager 5.3 software was used to calculate the odds ratio (OR) and 95% confidence interval (95% CI) for meta-analysis. Publication bias was investigated using the funnel plots, Begg's and Egger's publication bias plots. Twenty-one eligible studies were included to investigate the association between HSV-1 and AD. The results of the meta-analysis indicated that HSV-1 infection is a risk factor for AD (OR = 1.39, 95% CI = (1.14-1.69), P < 0.05)). In the subgroup analysis, the pooled ORs of HSV-1 infection associated with AD were 1.28 (95% CI: 0.74-2.22) in literature prior to 2010;1.44 (95% CI: 1.14-1.82) in literature after 2010; 1.27(95% CI: 1.01-1.60) in studies from Europe; 1.22(95% CI: 0.66-2.27) in studies from North America;1.89 (95% CI: 1.19-3.02) in studies from Asia; 1.38 (95% CI: 1.10-1.74) in the clinical diagnosis group; 1.52 (95% CI: 0.84-2.74) in the autopsy group. The pooled OR of APOE4 positivity and AD risk was 5.51 (95% CI: 4.33-7.01). The association between HCMV and AD was analyzed in seven studies. The pooled result showed that HCMV infection is not a risk factor for AD (OR = 0.83, 95% CI = 0.63-1.09). Our latest meta-analysis suggests that HSV-1 infection is a risk factor for the risk of AD. Therefore, anti-HSV-1 infection can serve as a potential therapeutic strategy for control of AD incidence. There is insufficient evidence to support association between HCMV and AD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adiponectin mediated metabolic and sphingolipid alterations in preventing endothelial dysfunction.","authors":"Vinnyfred Vincent, Himani Thakkar, Atanu Sen, Ashutosh Bansal, Ujjalkumar Subhash Das, Abishek Gunasekaran, Neerja Bhatla, Thirumurthy Velpandian, Archna Singh","doi":"10.1007/s11010-025-05268-1","DOIUrl":"https://doi.org/10.1007/s11010-025-05268-1","url":null,"abstract":"<p><p>Endothelial dysfunction is an early indicator of atherosclerosis. Adiponectin, a hormone secreted by adipose tissue with insulin-sensitizing and anti-inflammatory properties, offers protection against atherosclerosis. This study investigated the metabolic and sphingolipid alterations in endothelial cells linked to the protective effects of adiponectin against endothelial dysfunction. Human Umbilical Endothelial Cells (HUVECs) were treated with Tumor Necrosis Factor-alpha (TNF-α) to induce endothelial dysfunction. AdipoRon and SKI-I were used to study the effects of adiponectin and sphingosine kinase inhibition in HUVECs. Metabolic changes and sphingolipid alterations were assessed to understand changes in lipid metabolism, and RNA sequencing was used to quantify the transcriptomics changes. TNF-α treatment significantly upregulated glycolysis and downregulated long-chain fatty acid oxidation and mitochondrial ATP production, while AdipoRon co-treatment partially reversed these metabolic effects. In HUVECs, TNF-α treatment increased intracellular C16 and C18 ceramides and Sphingosine 1-Phosphate (S1P) while decreasing extracellular S1P. AdipoRon Co-treatment reversed these effects; AdipoRon also reversed the transcriptional changes induced by TNF-α. Sphingosine kinase inhibition in HUVECs led to mitochondrial dysfunction at the metabolic and transcriptional levels. This study provides insights into potential therapeutic strategies targeting endothelial metabolism while unraveling a novel mitochondrial modulation mediated by sphingosine kinases in endothelial cells.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}