Molecular and Cellular Biochemistry最新文献

{"title":"Retraction Note: Glutamine synthetase regulation by dexamethasone, RU486, and compound A in astrocytes derived from aged mouse cerebral hemispheres is mediated via glucocorticoid receptor.","authors":"Theodosia Kazazoglou, Christina Panagiotou, Chrysovalantou Mihailidou, Ioanna Kokkinopoulou, Anna Papadopoulou, Paraskevi Moutsatsou","doi":"10.1007/s11010-025-05295-y","DOIUrl":"10.1007/s11010-025-05295-y","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4883"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033704","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":"The interplay between autophagy and programmed cell death in osteoarthritis: insights into mechanisms and therapeutic targets.","authors":"Hong Wang, Jing Zhou, Yifan Lu, Hua Gao, Eryu Ning, Xing Yang, Yuefeng Hao, Dan Hu","doi":"10.1007/s11010-025-05279-y","DOIUrl":"10.1007/s11010-025-05279-y","url":null,"abstract":"<p><p>Osteoarthritis is a common degenerative joint disorder characterized by cartilage damage causing pain and movement impairment. Its progression involves inflammatory responses, metabolic abnormalities, and cell death pathways including autophagy. This review elucidates the regulatory mechanisms of autophagy in programmed cell death and its impact on osteoarthritis. Studies demonstrate that autophagy can regulate apoptosis, necroptosis and other death pathways through specific components, distinguishing ''autophagy-mediated cell death'' from the direct elimination mechanism of ''autophagy-dependent cell death''. In osteoarthritis, autophagy participates in cartilage degeneration and joint inflammation by modulating inflammatory factors and stress responses. Understanding the dual regulatory mechanisms of autophagy provides theoretical foundations for developing targeted therapeutic strategies. This article systematically compares pathway characteristics of different autophagy-related cell death types, proposing that precise regulation of autophagy-mediated death processes may emerge as a novel approach to protect cartilage and delay disease progression. These research advances offer crucial theoretical support for precision medicine in osteoarthritis management.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4627-4646"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008310","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":"Human umbilical cord mesenchymal stem cell-derived exosomes inhibit inflammation and fibrotic scar formation after intracerebral hemorrhage.","authors":"Aobo Zhang, Zhanzhan Zhang, Rongge Liu, Zongmao Zhao, Liqiang Liu","doi":"10.1007/s11010-025-05259-2","DOIUrl":"10.1007/s11010-025-05259-2","url":null,"abstract":"<p><p>Human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-ex) have emerged as a promising alternative to whole-cell therapies due to their minimal immunogenicity and tumorigenicity. Pentraxin 3 (PTX3) acts as an inflammatory marker and pattern recognition receptor, playing a critical role in promoting tumor progression and inflammatory diseases. Fibrotic scars resulting from cerebral hemorrhage can impair motor and sensory functions, leading to poor prognosis. This study aimed to investigate whether hUCMSC-ex regulate matrix metalloproteinase-3 (MMP3) expression via the PTX3/Toll-like receptor 4 (TLR4)/nuclear factor κB (NF-κB) pathway, thereby inhibiting inflammation and fibrotic scar formation following intracerebral hemorrhage and ultimately promoting the recovery of nerve function. A stereotactic technique was used to inject type IV collagenase (1 μL) into the striatum of rats, establishing an animal model of hemorrhagic stroke. Concurrently, hUCMSC-ex were administered via the tail vein at a dosage of 200 μg. In vitro, primary astrocytes were treated with hUCMSC-ex and subsequently stimulated with Hemin (20 μmol/mL) to create a cellular model of cerebral hemorrhage. The expression levels of PTX3, TLR4/NF-κB/MMP3 pathway proteins, and inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10), were assessed both in vivo and in vitro to investigate the effects of hUCMSC-ex on the inflammatory response and fibroblast migration. Neurological function in rats with cerebral hemorrhage was evaluated on days 1, 3, and 5 using the corner turn test, forelimb placement test, Longa score, and Bederson score. Additionally, real-time PCR was utilized to measure PTX3 mRNA expression following treatment with hUCMSC-ex. hUCMSC-ex inhibited MMP3 expression by downregulating the protein levels of PTX3, TLR4, NF-κB/P65, and p-P65. This action resulted in a reduction of pro-inflammatory cytokines TNF-α and IL-1β while simultaneously increasing the expression of the anti-inflammatory cytokine IL-10. Furthermore, hUCMSC-ex suppressed the inflammatory response, prevented fibroblast migration, and decreased MMP3 expression in the conditioned medium derived from primary astrocytes. Importantly, hUCMSC-ex improved behavioral performance in rats with intracerebral hemorrhage (ICH). hUCMSC-ex modulated the expression of MMP3 through the downregulation of PTX3, TLR4, NF-κB/P65, and p-P65. This regulatory mechanism contributed to a decrease in pro-inflammatory cytokines TNF-α and IL-1β, while concurrently enhancing the expression of the anti-inflammatory cytokine IL-10. Additionally, hUCMSC-ex effectively suppressed the inflammatory response, inhibited fibroblast migration, and reduced MMP3 expression in primary astrocyte-conditioned medium. Overall, hUCMSC-ex significantly improved behavioral performance in rats with ICH.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4829-4847"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144027282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL1-mediated m7G modification promotes colorectal cancer metastasis via stabilization of ICAM-1.","authors":"Shangwen Cai, Shuyi Mi, Jingyu Chen, Liming Shao, Xiaoyun Yang, Meng Xue","doi":"10.1007/s11010-025-05293-0","DOIUrl":"10.1007/s11010-025-05293-0","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common tumors worldwide, and metastatic CRC is likely to have a poor prognosis. N7-methylguanosine (m7G) is a common methylation modification that is catalyzed primarily by methyltransferase 1 (METTL1). However, the role of m7G in metastatic CRC remains unclear. The role of METTL1 in progressive CRC was initially explored using bioinformatics analysis. Subsequently, its relationship with CRC was further validated through in vitro and in vivo experiments. Potential downstream targets were identified through RNA-seq and quantitative real-time PCR (RT‒qPCR), and the underlying mechanisms were investigated using methylated RNA immunoprecipitation (MeRIP) and RNA degradation assays. Our results revealed that METTL1 is differentially expressed and significantly upregulated in metastatic CRC. This correlation was further confirmed by in vivo and in vitro experiments. RNA sequencing of CRC cells with METTL1 knockdown revealed that intercellular adhesion molecule-1 (ICAM-1) was a significant downstream target and could be stabilized by m7G modification. We revealed that METTL1 is significantly upregulated in metastatic CRC and plays a critical role in CRC progression by stabilizing ICAM-1 through m7G modification.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4769-4780"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12442457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impairment of platelet mitochondrial respiration in patients with chronic kidney disease with and without diabetes.","authors":"Glăvan Mihaela-Roxana, Stanciu-Lelcu Theia, Aburel Oana-Maria, Bînă Anca-Mihaela, Avram Vlad-Florian, Balint Lavinia, Gădălean Florica, Vlad Adrian, Sturza Adrian, Petrica Ligia, Muntean Mirela-Danina","doi":"10.1007/s11010-025-05280-5","DOIUrl":"10.1007/s11010-025-05280-5","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) and diabetic kidney disease (DKD) are major public health problems, and their burden is growing relentlessly with the aging of the global population. Their early recognition is now a public health priority, and there is an unmet need for the identification of specific biomarkers in minimally invasive or non-invasive samples. Mitochondrial dysfunction plays a pivotal role in the development and progression of both CKD and DKD and circulating platelets have emerged as an ideal candidate for the assessment of the respiratory function. The present study assessed mitochondrial respiration in platelets isolated from the peripheral blood of patients with DKD and CKD compared to healthy controls. The study included a total number of 89 subjects, as follows: 30 DKD patients divided into three subgroups based on the urinary albumin-to-creatinine ratio (uACR): 20 normoalbuminuric, 10 microalbuminuric, and 10 macroalbuminuric, 29 CKD patients (positive controls) and 20 healthy individuals (negative controls). Platelets were isolated by differential centrifugations and a high-resolution respirometry protocol was adapted to assess mitochondrial respiration dependent on complex I (CI) and complex II (CII). A significant reduction of the CI-supported active respiration was found in the normoalbuminuric DKD patients and further decreased in the microalbuminuric DKD subgroup. Both CI and CII-dependent coupled respiration and the maximal uncoupled respiration were significantly reduced in the macroalbuminuric DKD subgroup. In conclusion, mitochondrial respiration impairment in peripheral platelets is evident from the early stages of DKD. Moreover, platelet mitochondrial respiration was more severely impaired in patients with macroalbuminuric DKD as compared to those with CKD. Further, more extensive follow-up studies are warranted to determine whether platelet respiratory mitochondrial dysfunction could serve as a peripheral biomarker for kidney mitochondrial dysfunction and/or as a prognostic tool in DKD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4745-4755"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The multifaceted nature of SUMOylation in heart disease and its therapeutic potential.","authors":"Ying He, Zhijie Yang, Dan Guo, Cheng Luo, Qiaoqiao Liu, Lei Xian, Fan Yang, Chusheng Huang, Qingjun Wei","doi":"10.1007/s11010-025-05286-z","DOIUrl":"10.1007/s11010-025-05286-z","url":null,"abstract":"<p><p>SUMOylation (SUMO), a crucial post-translational modification, is implicated in the regulation of diverse biological processes and plays a pivotal role in both the maintenance of cardiac function and progression and treatment of heart disease. Here, we reviewed the mechanisms by which SUMO-related various aspects of cardiac function and disease, including cardiac hypertrophy, heart failure, ischemia-reperfusion injury, and myocardial infarction. Furthermore, we highlight its potential as a therapeutic target.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4725-4743"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971663","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":"Low-intensity exercise prevents cardiac inflammation through the NF-κB/TNFα pathway in insulin-resistant male rats.","authors":"Jelena Stanisic, Goran Koricanac, Tijana Culafic, Snjezana Romic, Mojca Stojiljkovic, Milan Kostic, Tamara Ivkovic, Snezana Tepavcevic","doi":"10.1007/s11010-025-05288-x","DOIUrl":"10.1007/s11010-025-05288-x","url":null,"abstract":"<p><p>Our previously published results have proven that low-intensity exercise, equivalent to brisk walking, is beneficial in managing cardiac insulin resistance in post-weaning male rats exposed to a fructose-rich diet. Still, its role in protecting against cardiac inflammation is unclear. This experiment was designed to investigate the preventive effect of low-intensity exercise on cardiac inflammation in male post-weaning rats exposed to a fructose-rich diet (10%). Male Wistar rats were randomly assigned to a sedentary control group, a sedentary group with fructose overload, and a fructose overload group subjected to treadmill exercise for nine weeks. Protein expression of cardiac inducible nitric oxide synthase (iNOS), matrix metalloproteinase 9, as well as cellular localization/phosphorylation of nuclear factor kappa B (NF-κB), and α1 and α2 subunits of sodium-potassium ATPase pump (Na/K-ATPase) was determined. Additionally, gene expression of tumor necrosis factor α (TNFα) and suppressor of cytokine signaling 3 (SOCS3) was examined. The results demonstrate that a chronic fructose-rich diet in sedentary rats elevates the expression of key inflammatory markers, including SOCS3, TNFα, NF-κB, and iNOS, as well as the plasma membrane α1 and α2 subunits. Exercise prevented alterations induced by a fructose-rich diet, except iNOS expression. Additionally, exercise increased the protein expression of the α1 and α2 subunits of Na/K-ATPase in the lysate of fructose-fed rats. These findings suggest that low-intensity exercise is an effective non-invasive strategy for cardioprotection, helping to prevent inflammation by modulating TNFα and NF-κB expression in insulin-resistant hearts of post-weaning male rats.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4757-4767"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033689","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":"Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.","authors":"Ana Grego, Cristiana Fernandes, Ivo Fonseca, Marina Dias-Neto, Raquel Costa, Adelino Leite-Moreira, Sandra Marisa Oliveira, Fábio Trindade, Rita Nogueira-Ferreira","doi":"10.1007/s11010-025-05289-w","DOIUrl":"10.1007/s11010-025-05289-w","url":null,"abstract":"<p><p>Endothelial cells (ECs) are arranged side-by-side to create a semi-permeable monolayer, forming the inner lining of every blood vessel (micro and macrocirculation). Serving as the first barrier for circulating molecules and cells, ECs represent the main regulators of vascular homeostasis being able to respond to environmental changes, either physical or chemical signals, by producing several factors that regulate vascular tone and cellular adhesion. Healthy endothelium has anticoagulant properties that prevent the adhesion of leukocytes and platelets to the vessel walls, contributing to resistance to thrombus formation, and regulating inflammation, and vascular smooth muscle cell proliferation. Many risk factors of cardiovascular diseases (CVDs) promote the endothelial expression of chemokines, cytokines, and adhesion molecules. The resultant endothelial activation can lead to endothelial cell dysfunction (ECD). In vitro models of ECD allow the study of cellular and molecular mechanisms of disease and provide a research platform for screening potential therapeutic agents. Even though alternative models are available, such as animal models or ex vivo models, in vitro models offer higher experimental flexibility and reproducibility, making them a valuable tool for the understanding of pathophysiological mechanisms of several diseases, such as CVDs. Therefore, this review aims to synthesize the currently available in vitro models regarding ECD, emphasizing CVDs. This work will focus on 2D cell culture models (endothelial cell lines and primary ECs), 3D cell culture systems (scaffold-free and scaffold-based), and 3D cell culture models (such as organ-on-a-chip). We will dissect the role of external stimuli-chemical and mechanical-in triggering ECD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4671-4695"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144044400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","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":"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":"4573-4586"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","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":"Alkaloids as neuroprotectors: targeting signaling pathways in neurodegenerative diseases.","authors":"Biswajit Kumar Utpal, Md Al Amin, Mehrukh Zehravi, Sherouk Hussein Sweilam, Uppuluri Varuna Naga Venkata Arjun, Y Bala Madhuri, Jeetendra Kumar Gupta, Lavanya Yaidikar, Tanuja Tummala, R Suseela, Akiladevi Durairaj, Konatham Teja Kumar Reddy, Ali Audah Fahaid Al Fahaid, Safia Obaidur Rab, Mohammed Saeed Almahjari, Talha Bin Emran","doi":"10.1007/s11010-025-05258-3","DOIUrl":"10.1007/s11010-025-05258-3","url":null,"abstract":"<p><p>Neurodegeneration is the progressive loss of neurons that results in neurodegenerative diseases (NDs). Currently, there are few effective treatments for NDs, such as Alzheimer's disease, Parkinson's disease, Multiple sclerosis, and Huntington's disease, which involve gradual neuronal death and cognitive deterioration. Alkaloids are naturally occurring molecules with a variety of biological properties. Recent studies have shown that these compounds may be able to modulate signaling pathways linked to many diseases. Alkaloids, with their antioxidant and neuroprotective properties, have the potential to treat neurodegeneration by simultaneously affecting multiple disease parts and modifying neuroinflammatory responses. These interact with various molecular targets, such as transcription factors, receptors, and enzymes involved in neuronal survival and homeostasis. The development of complete therapeutic techniques can be facilitated by alkaloid-based multi-target approaches, which challenge the intricate nature of neurodegenerative pathways. The review highlights the potential of alkaloid-based multi-target strategies in treating NDs and calls for further research to understand their clinical applications fully. Future studies should focus on finding neuroprotective alkaloids, investigating their mechanisms, and evaluating their therapeutic potential. Understanding how alkaloids interact with key pathways in NDs is essential for developing effective therapies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4587-4612"},"PeriodicalIF":3.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795855","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}