Bin Xu, Xiaobing Niu, Xiangxiang Zhang, Jun Tao, Deyao Wu, Zidun Wang, Pengchao Li, Wei Zhang, Hongfei Wu, Ninghan Feng, Zengjun Wang, Lixin Hua, Xinru Wang
{"title":"Correction to: miR-143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS.","authors":"Bin Xu, Xiaobing Niu, Xiangxiang Zhang, Jun Tao, Deyao Wu, Zidun Wang, Pengchao Li, Wei Zhang, Hongfei Wu, Ninghan Feng, Zengjun Wang, Lixin Hua, Xinru Wang","doi":"10.1007/s11010-025-05333-9","DOIUrl":"10.1007/s11010-025-05333-9","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5545-5548"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475977","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-brain-immune axis implications for mental health and disease.","authors":"Hadi Nasiri, Zahra Valedkarimi, Morteza Akbari","doi":"10.1007/s11010-025-05325-9","DOIUrl":"10.1007/s11010-025-05325-9","url":null,"abstract":"<p><p>Significantly affecting mental health, the gut-brain-immune axis shows a complicated interaction between the gastrointestinal tract, immune system, and central nervous system. Maintaining immunological homeostasis and brain function depends on gut bacteria, which are crucial due to their varied microbial populations. Along this axis, communication takes place via immunological responses, microbial metabolites, and brain pathways. Mental health issues like stress, sadness, autism spectrum disorders (ASD), and schizophrenia are linked to dysbiosis and inflammation. Restoring microbial balance and enhancing mental health outcomes show promise from therapeutic approaches, including probiotics, prebiotics, dietary changes, and pharmaceutical and non-pharmacological therapies. Future studies should concentrate on clarifying the gut-brain-immune axis mechanics, creating individualized treatments, and applying results into clinical use. By tackling their underlying causes and encouraging general well-being, this combined approach presents fresh paths for treating mental health problems.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5243-5265"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275393","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}
Fan Peng, Yanping Long, Taolin Zheng, Minghui Leng, Hui Deng
{"title":"Bone marrow mesenchymal stem cells promote the recovery of stroke in rats with type 2 diabetes mellitus by inhibiting the activation of TLR4/NF-κB signaling pathway.","authors":"Fan Peng, Yanping Long, Taolin Zheng, Minghui Leng, Hui Deng","doi":"10.1007/s11010-025-05332-w","DOIUrl":"10.1007/s11010-025-05332-w","url":null,"abstract":"<p><p>Ischemic stroke is a major complication of type 2 diabetes mellitus (T2DM), significantly contributing to increased mortality in T2DM patients. Bone marrow mesenchymal stem cells (BMSCs), known for their multidirectional differentiation potential, have shown therapeutic potential in treating ischemic stroke associated with T2DM; however, the underlying mechanisms remain unclear. This study aimed to investigate the therapeutic effects and mechanisms of BMSCs in T2DM-related ischemic stroke. A T2DM rat model was established and subjected to transient middle cerebral artery occlusion (MCAO) to induce ischemic stroke. BMSCs were administered to evaluate their effects on body weight, blood glucose levels, modified neurological severity score (mNSS), infarct volume, and blood-brain barrier (BBB) integrity in T2DM-MCAO rats. RNA sequencing was performed on brain tissues from T2DM-MCAO rats before and after BMSCs treatment to identify differentially expressed genes (DEGs). Functional enrichment analysis, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, quantitative real-time PCR, and western blot, were conducted to explore the underlying mechanisms. The results demonstrated that T2DM-MCAO rats exhibited increased body weight, elevated blood glucose levels, higher mNSS scores, larger brain infarct volumes, and BBB disruption, all of which were partially ameliorated by BMSCs treatment. Furthermore, BMSCs downregulated the expression of TLR4 and reduced the protein levels of p65 and phosphorylated p65 (p-p65), which were upregulated in T2DM-MCAO rats. Overexpression of TLR4 partially reversed the beneficial effects of BMSCs on functional outcomes, infarct volume, and BBB integrity. In conclusion, this study demonstrates that BMSCs alleviate T2DM-related ischemic stroke by suppressing TLR4 expression and inhibiting the TLR4/NF-κB signaling pathway, suggesting a potential therapeutic target for T2DM-associated ischemic stroke.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5447-5457"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275392","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":"Emerging trends in cardiovascular diseases: the impact of ferroptosis and cuproptosis on cardiomyocyte death.","authors":"Peijian Chen, Ping He, Xuejing Rao, Minglu Ding, Jieting Liu, Yanhui Chu, Yang Xiao","doi":"10.1007/s11010-025-05340-w","DOIUrl":"10.1007/s11010-025-05340-w","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) comprise a range of conditions affecting the heart and vasculature, encompassing ischemic heart disease (IHD), stroke, heart failure (HF), peripheral and aortic diseases, arrhythmias, and valvulopathy. Notably, the high prevalence rates of CVDs among younger populations warrant concern, emphasizing the importance of prevention and treatment. In recent years, ferroptosis, a novel form of cell death, has attracted significant research interest across various diseases. Similarly, cuproptosis, another cell death mechanism resulting from copper ion accumulation, has also been extensively studied. Cell death plays a crucial role in the development and maintenance of organisms, with both ferroptosis and cuproptosis closely associated with cell metabolism, signaling pathways, and drug resistance. Emerging evidence suggests that ferroptosis and cuproptosis are closely linked to the occurrence and progression of various diseases, including CVDs. The death of myocardial cells is pivotal in the pathophysiology of CVDs, with the roles of ferroptosis and cuproptosis in this process increasingly recognized. This article aims to summarize the molecular mechanisms and interactions of ferroptosis and cuproptosis, as well as their potential as novel targets for CVD treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5323-5344"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12515228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475978","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":"Piezo1: the Potential Novel Target for Radiation-induced Liver Fibrosis by Regulating FAP + fibroblasts.","authors":"Wentong Liu, Haochen Zou, Jiaying Wei, Lihua Dong, Wei Hou","doi":"10.1007/s11010-025-05327-7","DOIUrl":"10.1007/s11010-025-05327-7","url":null,"abstract":"<p><p>Radiation-induced liver fibrosis is a serious complication of radiotherapy in patients with liver cancer and is characterized by excessive deposition of the extracellular matrix (ECM). The activation of cancer-associated fibroblasts (CAFs) is central to this event. Piezo1 is a mechanoreceptor that is highly expressed in liver tissue and is closely related to the fibrotic process. CAFs are highly heterogeneous, and different cell populations perform different functions. Recent studies have shown that fap, an important surface marker of the CAF membrane, presumably plays a \"hub\" role upstream of α-smooth muscle actin (α-SMA). This article reviews the unique microenvironment of liver cancer and liver fibrosis and the role of piezo1 and CAFs in liver fibrosis. Building upon the foundational evidence, we formulate a hypothesis that radiation-induced ECM remodeling activates Piezo1-mediated mechanotransduction, driving HIF-1α/TGF-β pathways to stimulate CAF activation (manifested by FAP upregulation), which may synergistically aggravate liver fibrosis and hepatocarcinogenesis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5297-5308"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12515122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317478","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}
Zhizai Chen, Dalong Song, Shuting Huang, Jinyu Chao, Junhong Huang, Ming Luo, Shanyang He
{"title":"High IGFL2 regulates ovarian cancer progression and the tumor immune microenvironment via the Warburg effect.","authors":"Zhizai Chen, Dalong Song, Shuting Huang, Jinyu Chao, Junhong Huang, Ming Luo, Shanyang He","doi":"10.1007/s11010-025-05328-6","DOIUrl":"10.1007/s11010-025-05328-6","url":null,"abstract":"<p><p>This study aimed to explore the role and mechanism of insulin-like growth factor-like family member 2 (IGFL2) in ovarian cancer (OC) metastasis. Specifically, we focused on how IGFL2 regulates tumor cell energy metabolism and influences macrophage polarization to promote ovarian cancer metastasis. By conducting in vitro and in vivo experiments to elucidate the biological functions of IGFL2, this study aiming to identify new therapeutic targets for ovarian cancer treatment and provide a more effective treatment strategy. Our study revealed that the expression of IGFL2 was substantially upregulated in ovarian cancer metastases, and its high expression was positively correlated with the malignancy and metastatic potential of ovarian cancer. IGFL2 knockdown promoted mitochondrial oxidative phosphorylation and inhibited the Warburg effect, evidenced by increased oxygen consumption rate (OCR) and ATP production, and decreased glycolytic enzyme expression and lactate secretion. Concurrently, IGFL2 promoted M2 macrophage polarization via the STAT1/STAT6 signaling pathway, increasing the proportion of CD11b + CD206 + M2 cells and suppressing M1 polarization. In vivo, IGFL2 knockdown significantly inhibited tumor growth and metabolic reprogramming in xenograft models.These findings demonstrate that IGFL2 promotes OC metastasis through a dual mechanism: regulating metabolic reprogramming (Warburg effect) and influencing tumor-associated macrophage (TAM) polarization.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5485-5500"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475979","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 role of L-DOPA in neurological and neurodegenerative complications: a review.","authors":"Sudheendra Rao Kulkarni, Bothe Thokchom, Megha B Abbigeri, Santosh Mallikarjun Bhavi, Sapam Riches Singh, Nitish Metri, Ramesh Babu Yarajarla","doi":"10.1007/s11010-025-05324-w","DOIUrl":"10.1007/s11010-025-05324-w","url":null,"abstract":"<p><p>L-DOPA remains a cornerstone treatment for Parkinson's disease and is increasingly recognized for its role in various neurological and neurodegenerative disorders. As a direct precursor to dopamine, L-DOPA is synthesized from L-tyrosine through the action of tyrosine hydroxylase and is subsequently converted into dopamine via aromatic L-amino acid decarboxylase. Its ability to cross the blood-brain barrier (BBB) makes it a crucial therapeutic agent for restoring dopaminergic neurotransmission, thereby influencing motor function, cognition, and neuroprotection. Beyond Parkinson's, L-DOPA's therapeutic potential extends to neurodegenerative conditions such as Alzheimer's disease, Huntington's disease, multiple sclerosis, Lewy body dementia, and amyotrophic lateral sclerosis, where dopamine modulation plays a critical role. Furthermore, L-DOPA has demonstrated efficacy in neurological disorders including epilepsy, peripheral neuropathy, cerebrovascular diseases, and traumatic brain injury, suggesting broader neurobiological applications. However, long-term use is associated with challenges such as motor fluctuations, dyskinesias, and loss of therapeutic efficacy due to progressive neurodegeneration and alterations in dopaminergic pathways. Recent advancements in drug delivery systems, combination therapies, and nanotechnology, including plant-derived carbon dots, offer promising strategies to enhance L-DOPA's effectiveness while mitigating its limitations. This comprehensive review explores L-DOPA's synthesis, pharmacokinetics, mechanism of action, and its evolving role in neurological diseases, while highlighting ongoing challenges and future directions for optimizing its clinical application.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5221-5242"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248705","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":"Updated insights on ASK1 signaling: mechanisms, regulation, and therapeutic potential in diseases.","authors":"Divyanshi Thakur, Aniket Nandi, Yash Kumar Gaur, Karthikeyan Chandrabose, Digambar Kumar Waiker, Ghanshyam Das Gupta, Kalicharan Sharma","doi":"10.1007/s11010-025-05330-y","DOIUrl":"10.1007/s11010-025-05330-y","url":null,"abstract":"<p><p>Apoptosis signal-regulating kinase 1 (ASK1) is a serine-threonine kinase, that is a member of the mitogen-activated protein kinase kinase (MAP3K) family, which is expressed or incorporated in nucleated cells which leads to the activation of multiple mitogen-activated protein kinases (MAPK) to regulate cell stress, tumour necrosis factor-α (TNF-α) ligand, lipopolysaccharides and apoptosis. ASK1 gets activated by the ROS, oxidative stress, endoplasmic stress (ER) and various inflammatory cytokines. Dysregulation of ASK1 can lead to various diseases like neurodegenerative disease, cardiovascular disease, cancer, and various other metabolic diseases such as diabetes. This review summarizes ASK1's structure, its family, regulation, and its dual role in disease, highlighting its therapeutic potential for oxidative stress and inflammation-driven conditions while emphasizing the need for further clinical research. Inhibition of ASK1 demonstrates promising potential in treating fibrosis and various other diseases. We also discuss the dual role of ASK1 in both cancer initiation and suppression. Additionally, we explore ASK1 as a therapeutic target in diseases driven by oxidative stress and inflammation, emphasizing the need for further research to support its clinical translation.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5267-5296"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294109","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}
Kai Cui, Wanjun He, Na Huang, Songshan Zhu, Dan Jiang, Weiqiang Yang, Yiwei Zeng, Muhammad Asad Farooq, Guangxian Xu
{"title":"The challenges and progress of CAR-T cell therapy in the treatment of solid tumors.","authors":"Kai Cui, Wanjun He, Na Huang, Songshan Zhu, Dan Jiang, Weiqiang Yang, Yiwei Zeng, Muhammad Asad Farooq, Guangxian Xu","doi":"10.1007/s11010-025-05329-5","DOIUrl":"10.1007/s11010-025-05329-5","url":null,"abstract":"<p><p>Current traditional cancer treatment methods include surgery, chemotherapy, radiotherapy, etc., which lack targeted killing functions and may damage normal tissues. Immunotherapy, targeted therapy, and personalized medicine have become promising methods for cancer treatment, providing more precise and effective treatment for patients. Among them, chimeric antigen receptor (CAR)-T cell therapy utilizes the immune system's T cells to recognize and attack tumor cells, showing promising therapeutic prospects. The FDA has approved CAR-T therapy for treating B-cell acute lymphoblastic leukemia, large B-cell lymphoma, and multiple myeloma, targeting CD-19 and B-cell maturation antigens. Despite success in hematologic cancers, CAR-T technology faces challenges in solid tumors, including a lack of reliable tumor-associated antigens, hypoxic cores, immunosuppressive tumor environments, enhanced reactive oxygen species, and decreased T cell infiltration. This review covers the advantages and disadvantages of various immunotherapy methods, highlights CAR-T therapy's evolution, summarizes CAR-T therapy's current status, lists promising therapeutic targets, and emphasizes the challenges CAR-T cell therapy faces.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5345-5367"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475981","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}