Molecular and Cellular Biochemistry最新文献

{"title":"MicroRNA-122 regulates inflammatory and autophagic proteins by downregulating pyruvate kinase M2 in non-alcoholic fatty liver disease.","authors":"Md Musa Hossain, Amit K Mishra, Ajay K Yadav, Akanksha, Md Ismail, Teja Naveen Sata, Amrendra K Sah, Abdullah Al Mohit, Senthil K Venugopal","doi":"10.1007/s11010-024-05174-y","DOIUrl":"https://doi.org/10.1007/s11010-024-05174-y","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is one of the serious global health concerns, leading to non-alcoholic steatohepatitis (NASH), and to hepatocellular carcinoma (HCC). Despite its prevalence, the molecular mechanisms regulating NAFLD progression remain elusive. The present study aims to determine role of microRNA-122-mediated regulation of pyruvate kinase M2 (PKM2) on regulating inflammatory and autophagic proteins during the pathogenesis of NAFLD. Huh7 cells were incubated with free fatty acids (FFAs) or transfected with single guide RNA to PKM2 containing CRISPR-Cas9 system or miR-122 for up to 72 h. C57BL/6 mice were fed with sham-operated control, choline sufficient L-amino acid defined (CSAA) or choline-deficient L-amino acid defined (CDAA) diet for 6, 18, 32 and 54 weeks. The RNA or protein was isolated from the Huh7 cells and the liver tissue of the mice. RT-PCR was performed for miR-122 expression and Western blots were performed for PKM2, iNOS, COX2, Beclin-1, Atg7 and LC3-II. FFAs induced the expression of PKM2, iNOS and COX2, while decreased the expression of miR-122, Beclin-1, Atg7 and LC3-II. Overexpression of miR-122 resulted in decreased PKM2, iNOS and COX2 and increased Beclin-1, Atg7 and LC3-II. Silencing of PKM2 led to decreased iNOS and COX2 and increased Beclin-1, Atg7 and LC3-II. In CDAA fed-mice, there was a significant increase in PKM2, iNOS and COX2 and decreased miR-122, Beclin-1, Atg7 and LC3-II. The data showed that FFAs downregulated miR-122 expression, which resulted in the upregulation of PKM2, which in turn upregulated inflammatory proteins and downregulated autophagic proteins during the pathogenesis of NAFLD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770427","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":"FOXM1-activated IGF2BP3 promotes cell malignant phenotypes and M2 macrophage polarization in hepatocellular carcinoma by inhibiting ferroptosis via stabilizing RRM2 mRNA in an m6A-dependent manner.","authors":"Heng Gao, Lei Shi, Jinfeng Liu, Yingren Zhao, Fenjing Du, Yingli He, Xin Yang, Ning Song, Juan Wen, Gezhi Zheng","doi":"10.1007/s11010-024-05170-2","DOIUrl":"https://doi.org/10.1007/s11010-024-05170-2","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis has a crucial role in human carcinogenesis. N6-methyladenosine (m6A) reader insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) suppresses ferroptosis of hepatocellular carcinoma (HCC) cells. Here, we examined the effects and molecular determinants of IGF2BP3-mediated ferroptosis on malignant behaviors of HCC cells.</p><p><strong>Methods: </strong>Ferroptosis was evaluated by measuring the levels of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), and lipid ROS. HCC cell malignant phenotypes were evaluated by colony formation assay, wound healing assay, and transwell invasion assay. The CD206⁺ M2-like macrophages were assessed by flow cytometry. m6A RNA immunoprecipitation (MeRIP) was applied to assess the m6A modification of ribonucleotide reductase regulatory subunit M2 (RRM2). RNA immunoprecipitation (RIP) assay was performed to evaluate the interaction of IGF2BP3 and RRM2. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were conducted to confirm the interaction between forkhead box M1 (FOXM1) and IGF2BP3.</p><p><strong>Results: </strong>Human HCC tumors showed increased expression of IGF2BP3 compared with adjacent normal tissues. Disruption of IGF2BP3 promoted cell ferroptosis. Moreover, disruption of IGF2BP3 hindered HCC cell growth, invasiveness, and motility and impeded THP1-derived macrophage M2 polarization and migration by inducing ferroptosis. Additionally, IGF2BP3 disruption repressed xenograft growth in vivo. Mechanistically, IGF2BP3 enhanced RRM2 mRNA stability and elevated its protein expression by reading its m6A modification. Overexpression of RRM2 reversed sh-IGF2BP3-mediated ferroptosis and weakened sh-IGF2BP3-mediated suppression of HCC cell malignant phenotypes and macrophage M2 polarization. Furthermore, IGF2BP3 was a downstream target of FOXM1, and knockdown of FOXM1 induced ferroptosis and inhibited cell malignant phenotypes by downregulating IGF2BP3.</p><p><strong>Conclusion: </strong>FOXM1-induced IGF2BP3 upregulation promotes HCC cell malignant behaviors and macrophages M2 polarization by repressing ferroptosis via m6A-dependent regulation of RRM2 mRNA. Targeting FOXM1/IGF2BP3/RRM2 to enhance ferroptosis might be exploited as a potent therapeutic strategy for HCC.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770424","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":"Mitochondrial dysfunction in pregnancy loss: a review.","authors":"Lingjing Lu, Xinyue Huang, Yuqian Shi, Yue Jiang, Yanhua Han, Yuehui Zhang","doi":"10.1007/s11010-024-05171-1","DOIUrl":"https://doi.org/10.1007/s11010-024-05171-1","url":null,"abstract":"<p><p>A receptive endometrium, a healthy embryo, and harmonious communication between the mother and the embryo/fetus are necessary for a healthy and successful pregnancy. Pregnancy loss (PL) can be the outcome if there is a flaw in any of these critical developmental processes. Multiple risk factors contribute to PL, including genetic predispositions, uterine abnormalities, immune imbalances, endocrine dysfunctions, and environmental exposures, among others. Despite extensive investigations, more than half of women with recurrent pregnancy loss (RPL) lack identifiable risk factors, and causes of RPL remain elusive. To date, an accumulating body of evidence indicates that mitochondrial dysfunction in reproductive organs or cells is a potential underlying factor that may trigger PL. In this comprehensive review, we delve into the intricate relationship between mitochondrial dysfunction and PL, examining studies that focus on this connection in the context of diverse reproductive organs and cells, to unravel the interwoven links between these factors and gain a deeper understanding of their interconnectedness.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770444","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":"Coronary microthrombi in the failing human heart: the role of von Willebrand factor and PECAM-1.","authors":"Sawa Kostin, Theodoros Giannakopoulos, Manfred Richter, Florian Krizanic, Benjamin Sasko, Oliver Ritter, Nikolaos Pagonas","doi":"10.1007/s11010-024-04942-0","DOIUrl":"10.1007/s11010-024-04942-0","url":null,"abstract":"<p><p>The recognition of microthrombi in the heart microcirculation has recently emerged from studies in COVID-19 decedents. The present study investigated the ultrastructure of coronary microthrombi in heart failure (HF) due to cardiomyopathies that are unrelated to COVID-19 infection. In addition, we have investigated the role of von Willebrand factor (VWF) and PECAM-1 in microthrombus formation. We used electron microscopy to investigate the occurrence of microthrombi in patients with HF due to dilated (DCM, n = 7), inflammatory (MYO, n = 6) and ischemic (ICM, n = 7) cardiomyopathy and 4 control patients. VWF and PECAM-1 was studied by quantitative immunohistochemistry and Western blot. In comparison to control, the number of microthrombi was increased 7-9 times in HF. This was associated with a 3.5-fold increase in the number of Weibel-Palade bodies (WPb) in DCM and MYO compared to control. A fivefold increase in WPb in ICM was significantly different from control, DCM and MYO. In Western blot, VWF was increased twofold in DCM and MYO, and more than threefold in ICM. The difference between ICM and DCM and MYO was statistically significant. These results were confirmed by quantitative immunohistochemistry. Compared to control, PECAM-1 was by approximatively threefold increased in all groups of patients. This is the first study to demonstrate the occurrence of microthrombi in the failing human heart. The occurrence of microthrombi is associated with increased expression of VWF and the number of WPb, being more pronounced in ICM. These changes are likely not compensated by increases in PECAM-1 expression.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3437-3446"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139913060","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":"P4HA3 promotes colon cancer cell escape from macrophage phagocytosis by increasing phagocytosis immune checkpoint CD47 expression.","authors":"Hailang Zhou, Junwei Zou, Jingli Han, Aijun Zhou, Shu Huang","doi":"10.1007/s11010-024-04927-z","DOIUrl":"10.1007/s11010-024-04927-z","url":null,"abstract":"<p><p>Cancer immunotherapies have greatly changed the prospects for the therapy of many malignancies, including colon cancer. Macrophages as the effectors of cancer immunotherapy provide considerable promise for cancer treatment. Prolyl 4-hydroxylase subunit alpha 3 (P4HA3) plays a cancer-promoting role in a variety of cancers, including colon cancer. In the present work, we provided evidence for the first time that P4HA3 promoted colon cancer cell escape from macrophage phagocytosis, and preliminarily explored its possible molecular mechanism. Immunohistochemistry was used to detect the expression of P4HA3 in tissues. Bioinformatics methods were used to analyze the tumor public databases (including TCGA database and GEO database). Macrophage phagocytosis assay and flow cytometric analysis were used to detect the phagocytic capacity of macrophages. Western blot and qRT-PCR were used to detect the expression of related markers (such as P4HA3, CD47, CD24, IL-34, and M-CSF). First, we found that P4HA3 was significantly and highly expressed in both colon cancer tissues and cells, and that P4HA3 had a positive correlation with lymph node metastasis, Dukes stage and also strongly correlated with poorer survival. Subsequently, we found that P4HA3 was strongly associated with the macrophage infiltration level in colon cancer. Immediately we also found that decreasing P4HA3 expression promoted macrophage phagocytosis in colon cancer cells, whereas P4HA3 overexpression produced the opposite effect. Finally, we demonstrated that P4HA3 promoted the expression of cluster of differentiation 47 (CD47) in colon cancer cells. Moreover, P4HA3 caused colon cancer cells to secrete Interleukin 34 (IL34) and Macrophage colony stimulating factor (M-CSF), which further induced macrophages to differentiate to M2 type and thereby contributed to the progression of colon cancer. We have demonstrated that P4HA3-driven CD47 overexpression may act as an escape mechanism, causing colon cancer cells to evade phagocytosis from macrophages.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3355-3374"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139723371","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":"Functional activity and morphology of isolated rat cardiac mitochondria under calcium overload. Effect of naringin.","authors":"T A Kavalenia, E A Lapshina, T V Ilyich, Hu-Cheng Zhao, I B Zavodnik","doi":"10.1007/s11010-024-04935-z","DOIUrl":"10.1007/s11010-024-04935-z","url":null,"abstract":"<p><p>The function of mitochondria as a regulator of myocyte calcium homeostasis has been extensively discussed. The aim of the present work was further clarification of the details of modulation of the functional activity of rat cardiac mitochondria by exogenous Ca²⁺ ions either in the absence or in the presence of the plant flavonoid naringin. Low free Ca²⁺ concentrations (40-250 nM) effectively inhibited the respiratory activity of heart mitochondria, remaining unaffected the efficacy of oxygen consumption. In the presence of high exogenous Ca²⁺ ion concentrations (Ca²⁺ free was 550 µM), we observed a dramatic increase in mitochondrial heterogeneity in size and electron density, which was related to calcium-induced opening of the mitochondrial permeability transition pores (MPTP) and membrane depolarization (Ca²⁺free ions were from 150 to 750 µM). Naringin partially prevented Ca²⁺-induced cardiac mitochondrial morphological transformations (200 µM) and dose-dependently inhibited the respiratory activity of mitochondria (10-75 µM) in the absence or in the presence of calcium ions. Our data suggest that naringin (75 µM) promoted membrane potential dissipation, diminishing the potential-dependent accumulation of calcium ions by mitochondria and inhibiting calcium-induced MPTP formation. The modulating effect of the flavonoid on Ca²⁺-induced mitochondria alterations may be attributed to the weak-acidic nature of the flavonoid and its protonophoric/ionophoric properties. Our results show that the sensitivity of rat heart mitochondria to Ca²⁺ ions was much lower in the case of MPTP opening and much higher in the case of respiration inhibition as compared to liver mitochondria.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3329-3340"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139707228","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":"RETRACTED ARTICLE: Upregulation of MCL-1 by LUCAT1 through interacting with SRSF1 promotes the migration and invasion in non-small cell lung carcinoma.","authors":"Fang Fang, Mei Zhao, Xiaowei Jin, Zhixin Dong, Jiaxiao Wang, Jinming Meng, Sheng Xie, Wei Shi","doi":"10.1007/s11010-023-04851-8","DOIUrl":"10.1007/s11010-023-04851-8","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3305"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41163993","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":"Long non-coding RNAs in cancer: multifaceted roles and potential targets for immunotherapy.","authors":"Lokesh K Kadian, Deepika Verma, Neelam Lohani, Ritu Yadav, Shalu Ranga, Gulshan Gulshan, Sanghapriya Pal, Kiran Kumari, Shyam S Chauhan","doi":"10.1007/s11010-024-04933-1","DOIUrl":"10.1007/s11010-024-04933-1","url":null,"abstract":"<p><p>Cancer remains a major global health concern with high mortality rates mainly due to late diagnosis and poor prognosis. Long non-coding RNAs (lncRNAs) are emerging as key regulators of gene expression in human cancer, functioning through various mechanisms including as competing endogenous RNAs (ceRNAs) and indirectly regulating miRNA expression. LncRNAs have been found to have both oncogenic and tumor-suppressive roles in cancer, with the former promoting cancer cell proliferation, migration, invasion, and poor prognosis. Recent research has shown that lncRNAs are expressed in various immune cells and are involved in cancer cell immune escape and the modulation of the tumor microenvironment, thus highlighting their potential as targets for cancer immunotherapy. Targeting lncRNAs in cancer or immune cells could enhance the anti-tumor immune response and improve cancer immunotherapy outcomes. However, further research is required to fully understand the functional roles of lncRNAs in cancer and the immune system and their potential as targets for cancer immunotherapy. This review offers a comprehensive examination of the multifaceted roles of lncRNAs in human cancers, with a focus on their potential as targets for cancer immunotherapy. By exploring the intricate mechanisms underlying lncRNA-mediated regulation of cancer cell proliferation, invasion, and immune evasion, we provide insights into the diverse therapeutic applications of these molecules.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3229-3254"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139983279","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":"Neutrophil extracellular traps: a catalyst for atherosclerosis.","authors":"Yinyu Wang, Cuiping Wang, Jiayan Li","doi":"10.1007/s11010-024-04931-3","DOIUrl":"10.1007/s11010-024-04931-3","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs) are network-like structures released by activated neutrophils. They consist mainly of double-stranded DNA, histones, and neutrophil granule proteins. Continuous release of NETs in response to external stimuli leads to activation of surrounding platelets and monocytes/macrophages, resulting in damage to endothelial cells (EC) and vascular smooth muscle cells (VSMC). Some clinical trials have demonstrated the association between NETs and the severity and prognosis of atherosclerosis. Furthermore, experimental findings have shed light on the molecular mechanisms by which NETs contribute to atherogenesis. NETs play a significant role in the formation of atherosclerotic plaques. This review focuses on recent advancements in the understanding of the relationship between NETs and atherosclerosis. It explores various aspects, including the formation of NETs in atherosclerosis, clinical trials investigating NET-induced atherosclerosis, the mechanisms by which NETs promote atherogenesis, and the translational implications of NETs. Ultimately, we aim to propose new research directions for the diagnosis and treatment of atherosclerosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3213-3227"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139944306","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":"Melatonin antagonizes oxidative stress-induced apoptosis in retinal ganglion cells through activating the thioredoxin-1 pathway.","authors":"Shan Gao, Qiaochu Cheng, Yaguang Hu, Xiaojuan Fan, Chen Liang, Chen Niu, Qianyan Kang, Ting Wei","doi":"10.1007/s11010-024-04924-2","DOIUrl":"10.1007/s11010-024-04924-2","url":null,"abstract":"<p><p>This study aimed to explore the role of melatonin in oxidative stress-induced injury on retinal ganglion cells and the underlying mechanisms. The immortalized RGC-5 cells were treated with H₂O₂ to induce oxidative injury. Cell viability was measured by Cell Counting Kit-8, and apoptosis was determined by flow cytometry and western blot assays. Reactive oxygen species (ROS), lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels were examined to evaluate oxidative stress levels. In addition, Thioredoxin-1 (Trx1) was silenced in RGC-5 cells using small interfering RNA followed by signaling pathway examination to explore the underlying mechanisms of melatonin in alleviating oxidative injury. Melatonin pre-treatment significantly alleviated H₂O₂-induced apoptosis in RGC-5 cells. Melatonin also markedly reversed the upregulation of cleaved-caspase 3, cleaved-caspase 9, and Bax expression and downregulation of Bcl-2 expression induced by H₂O₂. Further analyses presented that melatonin significantly attenuated the increase of ROS, LDH, and MDA levels in RGC-5 cells after H₂O₂ treatment. Melatonin also abolished the downregulated expression of Superoxide dismutase type 1, Trx1, and Thioredoxin reductase 1, and the reduced activity of thioredoxin reductase in RGC-5 cells after H₂O₂ treatment. Notably, Trx1 knockdown significantly mitigated the protective effect of melatonin in alleviating H₂O₂-induced apoptosis and oxidative stress, while administration of compound C, a common inhibitor of c-Jun N-terminal kinase (JNK) signaling, partially reversed the effect of Trx1 silencing, thereby ameliorating the apoptosis and oxidative injury induced by H₂O₂ in RGC-5 cells. Melatonin could significantly alleviate oxidative stress-induced injury of retinal ganglion cells via modulating Trx1-mediated JNK signaling pathway.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3393-3404"},"PeriodicalIF":3.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139730059","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}