Molecular and Cellular Biochemistry最新文献

{"title":"The role of long noncoding ribonucleic acids in the central nervous system injury.","authors":"Min Huang, Xizhi Wang, Benson O A Botchway, Yong Zhang, Xuehong Liu","doi":"10.1007/s11010-023-04875-0","DOIUrl":"10.1007/s11010-023-04875-0","url":null,"abstract":"<p><p>Central nervous system (CNS) injury involves complex pathophysiological molecular mechanisms. Long noncoding ribonucleic acids (lncRNAs) are an important form of RNA that do not encode proteins but take part in the regulation of gene expression and various biological processes. Multitudinous studies have evidenced lncRNAs to have a significant role in the process of progression and recovery of various CNS injuries. Herein, we review the latest findings pertaining to the role of lncRNAs in CNS, both normal and diseased state. We aim to present a comprehensive clinical application prospect of lncRNAs in CNS, and thus, discuss potential strategies of lncRNAs in treating CNS injury.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66784077","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":"Disrupting of IGF2BP3-stabilized HK2 mRNA by MYO16-AS1 competitively binding impairs LUAD migration and invasion.","authors":"Peiwei Li, Haibo Ge, Jiangfeng Zhao, Yongjia Zhou, Jie Zhou, Peichao Li, Junwen Luo, Wenhao Zhang, Zhongxian Tian, Xiaogang Zhao","doi":"10.1007/s11010-023-04887-w","DOIUrl":"10.1007/s11010-023-04887-w","url":null,"abstract":"<p><p>Since invasive cancer is associated with poor clinical outcomes, exploring the molecular mechanism underlying LUAD progression is crucial to improve the prognosis of patients with advanced disease. Herein, we found that MYO16-AS1 is expressed mainly in lung tissue but is notably downregulated in LUAD tissues. Overexpression of MYO16-AS1 inhibited the migration and invasion of LUAD cells. Mechanistic studies indicated that H3^K27Ac modification mediated MYO16-AS1 transcription. Furthermore, we found that MYO16-AS1 competitively bound to the IGF2BP3 protein and in turn reduced IGF2BP3 protein binding to HK2 mRNA, decreasing HK2 mRNA stability and inhibiting glucose metabolism reprogramming and LUAD cell invasion in vitro and in vivo. The finding that the MYO16-AS1/IGF2BP3-mediated glucose metabolism reprogramming mechanism regulates HK2 expression provides novel insight into the process of LUAD invasion and suggests that MYO16-AS1 may be a therapeutic target for LUAD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11455711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470507","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":"Crosstalk between ferroptosis and macrophages: potential value for targeted treatment in diseases.","authors":"Wanxin Lan, Lei Yang, Xuelian Tan","doi":"10.1007/s11010-023-04871-4","DOIUrl":"10.1007/s11010-023-04871-4","url":null,"abstract":"<p><p>Ferroptosis is a newly identified form of programmed cell death that is connected to iron-dependent lipid peroxidization. It involves a variety of physiological processes involving iron metabolism, lipid metabolism, oxidative stress, and biosynthesis of nicotinamide adenine dinucleotide phosphate, glutathione, and coenzyme Q10. So far, it has been discovered to contribute to the pathological process of many diseases, such as myocardial infarction, acute kidney injury, atherosclerosis, and so on. Macrophages are innate immune system cells that regulate metabolism, phagocytize pathogens and dead cells, mediate inflammatory reactions, promote tissue repair, etc. Emerging evidence shows strong associations between macrophages and ferroptosis, which can provide us with a deeper comprehension of the pathological process of diseases and new targets for the treatments. In this review, we summarized the crosstalk between macrophages and ferroptosis and anatomized the application of this association in disease treatments, both non-neoplastic and neoplastic diseases. In addition, we have also addressed problems that remain to be investigated, in the hope of inspiring novel therapeutic strategies for diseases.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50162107","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 new promising target for hepatocellular carcinoma therapy.","authors":"Qiaoping Xu, Lanqi Ren, Ning Ren, Yibei Yang, Junjie Pan, Yu Zheng, Gang Wang","doi":"10.1007/s11010-023-04893-y","DOIUrl":"10.1007/s11010-023-04893-y","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the sixed most common malignant tumor in the world. The study for HCC is mired in the predicament confronted with the difficulty of early diagnosis and high drug resistance, the survival rate of patients with HCC being low. Ferroptosis, an iron-dependent cell death, has been discovered in recent years as a cell death means with tremendous potential to fight against cancer. The in-depth researches for iron metabolism, lipid peroxidation and dysregulation of antioxidant defense have brought about tangible progress in the firmament of ferroptosis with more and more results showing close connections between ferroptosis and HCC. The potential role of ferroptosis has been widely used in chemotherapy, immunotherapy, radiotherapy, and nanotherapy, with the development of various new drugs significantly improving the prognosis of patients. Based on the characteristics and mechanisms of ferroptosis, this article further focuses on the main signaling pathways and promising treatments of HCC, envisioning that existing problems in regard with ferroptosis and HCC could be grappled with in the foreseeable future.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138487951","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":"MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.","authors":"Teng Ge, Bo Ning, Yongqing Wu, Xiaolin Chen, Hongfei Qi, Haifang Wang, Mingjun Zhao","doi":"10.1007/s11010-023-04876-z","DOIUrl":"10.1007/s11010-023-04876-z","url":null,"abstract":"<p><p>MicroRNAs are single-stranded non-coding RNAs that participate in post-transcriptional regulation of gene expression, it is involved in the regulation of apoptosis after myocardial ischemia-reperfusion injury. For example, the alteration of mitochondrial structure is facilitated by MicroRNA-1 through the regulation of apoptosis-related proteins, such as Bax and Bcl-2, thereby mitigating cardiomyocyte apoptosis. MicroRNA-21 not only modulates the expression of NF-κB to suppress inflammatory signals but also activates the PI3K/AKT pathway to mitigate ischemia-reperfusion injury. Overexpression of MicroRNA-133 attenuates reactive oxygen species (ROS) production and suppressed the oxidative stress response, thereby mitigating cellular apoptosis. MicroRNA-139 modulates the extrinsic death signal of Fas, while MicroRNA-145 regulates endoplasmic reticulum calcium overload, both of which exert regulatory effects on cardiomyocyte apoptosis. Therefore, the article categorizes the molecular mechanisms based on the three classical pathways and multiple signaling pathways of apoptosis. It summarizes the targets and pathways of MicroRNA therapy for ischemia-reperfusion injury and analyzes future research directions.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50158339","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":"Effects of direct pulp capping with recombinant human erythropoietin and/or mineral trioxide aggregate on inflamed rat dental pulp.","authors":"Milos Papic, Suzana Zivanovic, Tamara Vucicevic, Miona Vuletic, Mirjana V Papic, Nevena Milivojević, Ana Mirić, Marina Miletic Kovacevic, Marko Zivanovic, Milan Stamenkovic, Vladimir Zivkovic, Slobodanka Mitrovic, Vladimir Jakovljevic, Biljana Ljujic, Milica Popovic","doi":"10.1007/s11010-023-04868-z","DOIUrl":"10.1007/s11010-023-04868-z","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the dental pulp responses to recombinant human erythropoietin (rhEPO) and/or mineral trioxide aggregate (MTA) in pulp capping of inflamed dental pulp in vivo.</p><p><strong>Materials and methods: </strong>In accordance with ARRIVE guidelines, pulp inflammation was induced by exposing the maxillary first molars (n = 64) of Wistar rats (n = 32) to the oral environment for two days. The exposed pulps were randomly assigned four groups based on the pulp capping material: rhEPO, MTA, MTA + rhEPO, or an inert membrane. An additional eight rats formed the healthy control group. After four weeks, the animals were euthanized, and histological, qRT-PCR, and spectrophotometric techniques were employed to analyze the left maxillary segments, right first maxillary molars, and blood samples, respectively. Statistical significance was set at p < 0.05 and < 0.001.</p><p><strong>Results: </strong>Pulp capping with rhEPO, MTA, or MTA + rhEPO resulted in lower inflammation and higher mineralization scores compared to untreated control. MTA + rhEPO group exhibited significantly decreased expression of tumor necrosis factor-alpha, and interleukin 1-beta, while MTA group showed substantially reduced expression of interferon-gamma. Both rhEPO and MTA + rhEPO groups presented elevated dentin matrix protein 1 levels compared to untreated control. Furthermore, pulp capping with rhEPO and/or MTA led to increased transforming growth factor-beta 1 expression and reductions of pro-inflammatory/immunoregulatory cytokine ratios and prooxidative markers. Pulp capping with rhEPO also resulted in increase of systemic antioxidative stress markers.</p><p><strong>Conclusion: </strong>Capping with rhEPO or MTA + rhEPO resulted in a favorable effect that was similar or even superior to that of MTA.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50162108","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":"NRF2 signaling pathway and telomere length in aging and age-related diseases.","authors":"Alessandro Medoro, Luciano Saso, Giovanni Scapagnini, Sergio Davinelli","doi":"10.1007/s11010-023-04878-x","DOIUrl":"10.1007/s11010-023-04878-x","url":null,"abstract":"<p><p>The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is well recognized as a critical regulator of redox, metabolic, and protein homeostasis, as well as the regulation of inflammation. An age-associated decline in NRF2 activity may allow oxidative stress to remain unmitigated and affect key features associated with the aging phenotype, including telomere shortening. Telomeres, the protective caps of eukaryotic chromosomes, are highly susceptible to oxidative DNA damage, which can accelerate telomere shortening and, consequently, lead to premature senescence and genomic instability. In this review, we explore how the dysregulation of NRF2, coupled with an increase in oxidative stress, might be a major determinant of telomere shortening and age-related diseases. We discuss the relevance of the connection between NRF2 deficiency in aging and telomere attrition, emphasizing the importance of studying this functional link to enhance our understanding of aging pathologies. Finally, we present a number of compounds that possess the ability to restore NRF2 function, maintain a proper redox balance, and preserve telomere length during aging.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11455797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71425042","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":"Cancer stem cells: advances in the glucose, lipid and amino acid metabolism.","authors":"Weina Kong, Yunge Gao, Shuhua Zhao, Hong Yang","doi":"10.1007/s11010-023-04861-6","DOIUrl":"10.1007/s11010-023-04861-6","url":null,"abstract":"<p><p>Cancer stem cells (CSCs) are a class of cells with self-renewal and multi-directional differentiation potential, which are present in most tumors, particularly in aggressive tumors, and perform a pivotal role in recurrence and metastasis and are expected to be one of the important targets for tumor therapy. Studies of tumor metabolism in recent years have found that the metabolic characteristics of CSCs are distinct from those of differentiated tumor cells, which are unique to CSCs and contribute to the maintenance of the stemness characteristics of CSCs. Moreover, these altered metabolic profiles can drive the transformation between CSCs and non-CSCs, implying that these metabolic alterations are important markers for CSCs to play their biological roles. The identification of metabolic changes in CSCs and their metabolic plasticity mechanisms may provide some new opportunities for tumor therapy. In this paper, we review the metabolism-related mechanisms of CSCs in order to provide a theoretical basis for their potential application in tumor therapy.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50162106","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":"Role of exosome-derived miRNAs in diabetic wound angiogenesis.","authors":"Wen-Ting Chen, Yi Luo, Xue-Mei Chen, Jian-Hui Xiao","doi":"10.1007/s11010-023-04874-1","DOIUrl":"10.1007/s11010-023-04874-1","url":null,"abstract":"<p><p>Chronic wounds with high disability are among the most common and serious complications of diabetes. Angiogenesis dysfunction impair wound healing in patients with diabetes. Compared with traditional therapies that can only provide symptomatic treatment, stem cells-owing to their powerful paracrine properties, can alleviate the pathogenesis of chronic diabetic wounds and even cure them. Exosome-derived microRNAs (miRNAs), important components of stem cell paracrine signaling, have been reported for therapeutic use in various disease models, including diabetic wounds. Exosome-derived miRNAs have been widely reported to be involved in regulating vascular function and have promising applications in the repair and regeneration of skin wounds. Therefore, this article aims to review the current status of the pathophysiology of exosome-derived miRNAs in the diabetes-induced impairment of wound healing, along with current knowledge of the underlying mechanisms, emphasizing the regulatory mechanism of angiogenesis, we hope to document the emerging theoretical basis for improving wound repair by restoring angiogenesis in diabetes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61563953","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":"Exercise training decreases the load and changes the content of circulating SDS-resistant protein aggregates in patients with heart failure with reduced ejection fraction.","authors":"Marisol Gouveia, Cristine Schmidt, Priscilla Gois Basilio, Susana S Aveiro, Pedro Domingues, Ke Xia, Wilfredo Colón, Rui Vitorino, Rita Ferreira, Mário Santos, Sandra I Vieira, Fernando Ribeiro","doi":"10.1007/s11010-023-04884-z","DOIUrl":"10.1007/s11010-023-04884-z","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) often disrupts the protein quality control (PQC) system leading to protein aggregate accumulation. Evidence from tissue biopsies showed that exercise restores PQC system in HF; however, little is known about its effects on plasma proteostasis.</p><p><strong>Aim: </strong>To determine the effects of exercise training on the load and composition of plasma SDS-resistant protein aggregates (SRA) in patients with HF with reduced ejection fraction (HFrEF).</p><p><strong>Methods: </strong>Eighteen patients with HFrEF (age: 63.4 ± 6.5 years; LVEF: 33.4 ± 11.6%) participated in a 12-week combined (aerobic plus resistance) exercise program (60 min/session, twice per week). The load and content of circulating SRA were assessed using D2D SDS-PAGE and mass spectrometry. Cardiorespiratory fitness, quality of life, and circulating levels of high-sensitive C-reactive protein, N-terminal pro-B-type natriuretic peptide (NT-proBNP), haptoglobin and ficolin-3, were also evaluated at baseline and after the exercise program.</p><p><strong>Results: </strong>The exercise program decreased the plasma SRA load (% SRA/total protein: 38.0 ± 8.9 to 36.1 ± 9.7%, p = 0.018; % SRA/soluble fraction: 64.3 ± 27.1 to 59.8 ± 27.7%, p = 0.003). Plasma SRA of HFrEF patients comprised 31 proteins, with α-2-macroglobulin and haptoglobin as the most abundant ones. The exercise training significantly increased haptoglobin plasma levels (1.03 ± 0.40 to 1.11 ± 0.46, p = 0.031), while decreasing its abundance in SRA (1.83 ± 0.54 × 10¹¹ to 1.51 ± 0.59 × 10¹¹, p = 0.049). Cardiorespiratory fitness [16.4(5.9) to 19.0(5.2) ml/kg/min, p = 0.002], quality of life, and circulating NT-proBNP [720.0(850.0) to 587.0(847.3) pg/mL, p = 0.048] levels, also improved after the exercise program.</p><p><strong>Conclusion: </strong>Exercise training reduced the plasma SRA load and enhanced PQC, potentially via haptoglobin-mediated action, while improving cardiorespiratory fitness and quality of life of patients with HFrEF.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11455743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71413087","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}