Experimental cell research最新文献

{"title":"RPF2 and CARM1 cooperate to enhance colorectal cancer metastasis via the AKT/GSK-3β signaling pathway","authors":"Cong Cheng ,&nbsp;KeMing Zhang ,&nbsp;MaCheng Lu ,&nbsp;Yuan Zhang ,&nbsp;Tong Wang ,&nbsp;Ye Zhang","doi":"10.1016/j.yexcr.2024.114374","DOIUrl":"10.1016/j.yexcr.2024.114374","url":null,"abstract":"<div><div>RPF2 plays a crucial role in promoting epithelial-mesenchymal transition (EMT) and regulating metastasis in colorectal cancer (CRC). By analyzing data from the TCGA and GEO databases, we observed significantly elevated RPF2 expression in CRC, which correlated with EMT markers. Further investigations using stable RPF2 overexpression and knockdown cell lines demonstrated that RPF2 facilitates EMT activation through the AKT/GSK-3β signaling pathway. Notably, CARM1 was identified as a key downstream effector of RPF2. Selective inhibition of CARM1 effectively suppressed the activation of the AKT/GSK-3β pathway and EMT induced by RPF2 overexpression. Both <em>in vitro</em> and <em>in vivo</em> experiments confirmed that RPF2 expression levels positively correlate with the metastatic potential of CRC cells. Moreover, treatment with a CARM1 inhibitor significantly reduced the invasive and migratory capabilities of RPF2-overexpressing cells. These findings suggest that RPF2 drives CRC metastasis by modulating EMT via the AKT/GSK-3β pathway, with CARM1 serving as a critical mediator, offering potential therapeutic targets for CRC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114374"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nucleostemin interacts with SMAD3 promoting tumor metastasis","authors":"Xuling Sun ,&nbsp;Jiageng He ,&nbsp;Yujiang Li ,&nbsp;Zhiqiang Chu ,&nbsp;Lei Zhu ,&nbsp;Hui Zhang ,&nbsp;Xiangwei Wu","doi":"10.1016/j.yexcr.2024.114362","DOIUrl":"10.1016/j.yexcr.2024.114362","url":null,"abstract":"<div><div>SMAD3 plays a crucial role in TGF-β, regulating various normal developmental mechanisms and disease pathogenesis. Here, we report that SMAD3 directly interacts with Nucleostemin (NS), leading to nuclear translocation and affecting SMAD3 activity after TGF-β1 stimulation. Moreover, NS acts as a competitor, preventing PPM1A from recognizing and dephosphorylating SMAD3. Experimental investigations have demonstrated that NS significantly enhances cellular migration and invasion by promoting the EMT mechanism in vitro. NS knockdown notably suppresses tumor metastasis in the lungs and liver in vivo. Importantly, NS expression is significantly elevated in numerous human malignancies, correlating with a poorer prognosis. The collective evidence from these studies suggests that <span>NS</span> exhibits oncogenic characteristics, supporting further exploration of <span>NS</span> as a potential target for tumor treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114362"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPC-3 in hepatocellular carcinoma; A novel biomarker and molecular target","authors":"Hamed Azhdari Tehrani ,&nbsp;Masood Zangi ,&nbsp;Mobina Fathi ,&nbsp;Kimia Vakili ,&nbsp;Moustapha Hassan ,&nbsp;Elham Rismani ,&nbsp;Nikoo Hossein-Khannazer ,&nbsp;Massoud Vosough","doi":"10.1016/j.yexcr.2024.114391","DOIUrl":"10.1016/j.yexcr.2024.114391","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a global health issue due to its late diagnosis and high recurrence rate. The early detection and diagnosis of HCC with specific and sensitive biomarkers and using novel treatment approaches to improve patient outcomes are essential. Glypican-3 (GPC-3) is a cell surface proteoglycan that is overexpressed in many tumors, including HCC. GPC-3 could be used as a specific biomarker for HCC early detection and could be a potential target for precise therapeutic strategies. Effective identification of GPC-3 could improve both diagnosis and targeted therapy of HCC. Moreover, targeted therapy using GPC-3 could result in a better treatment outcome. Recently, GPC3-targeted therapies have been used in different investigational therapeutic approaches like bi-specific/monoclonal antibodies, peptide vaccines, and CAR T cell therapies. This study aims to highlight the theranostic potential of GPC-3 as a novel biomarker for early detection and as a potential molecular target for HCC treatment as well.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114391"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Müller glia in short-term dark adaptation of the Austrolebias charrua retina: Cell proliferation and cytoarchitecture","authors":"Laura Herrera-Astorga ,&nbsp;Stephanie Silva ,&nbsp;Inés Berrosteguieta ,&nbsp;Juan Carlos Rosillo ,&nbsp;Anabel Sonia Fernández","doi":"10.1016/j.yexcr.2024.114394","DOIUrl":"10.1016/j.yexcr.2024.114394","url":null,"abstract":"<div><div>Fish with unique life cycles offer valuable insights into retinal plasticity, revealing mechanisms of environmental adaptation, cell proliferation, and thus, potentially regeneration. The variability of the environmental factors to which Austrolebias annual fishes are exposed has acted as a strong selective pressure shaping traits such as nervous system plasticity. This has contributed to adaptation to their extreme conditions including the decreased luminosity as ponds dry out. In particular, the retina of <em>A. charrua</em> has been shown to respond to 30 days of decreased luminosity by exacerbating cell proliferation Now, we aimed to determine the cellular component of the retina involved in shorter-term responses. To this end, we performed 5-bromo-2′-deoxyuridine (BrdU) experiments, exposing adult fish to a short period (11 days) of constant darkness. Strikingly, in control conditions, neurogenesis in the inner nuclear and ganglion cell layer in the differentiated retina was detected. In constant darkness, we observed an effect on inner nuclear layer cell proliferation and changes in retinal cytoarchitecture of the retina with cell clusters located in the inner plexiform layer. Additionally, increased BLBP (brain lipid-binding protein) presence was detected in darkness, which has been previously associated with immature and reactivated Müller glia. Thus, our results suggest that the <em>A. charrua</em> retina can respond to environmental changes via rapid activation of progenitor cells in the INL, namely the Müller glia This leads us to hypothesize, that cell proliferation and neurogenesis might contribute to the responses to the functional needs of organisms, potentially playing an adaptive role.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114394"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FoxC1 activates Notch3 signaling to promote the inflammatory phenotype of keloid fibroblasts and aggravates keloid","authors":"Yin Wang ,&nbsp;Zhengguo Xia ,&nbsp;Wengting Wang ,&nbsp;Jingsong Zhang ,&nbsp;Chao Hu ,&nbsp;Fan Wang ,&nbsp;Fei Zhu ,&nbsp;Lin sen Fang ,&nbsp;Jun Wang ,&nbsp;Xiaojing Li","doi":"10.1016/j.yexcr.2024.114402","DOIUrl":"10.1016/j.yexcr.2024.114402","url":null,"abstract":"<div><div>Keloids are disfiguring proliferative scars, and their pathological mechanisms are still unclear. We have previously established that FoxC1 plays a significant role in rheumatoid arthritis and osteoarthritis, but its molecular mechanisms in pathological scar formation remain elusive. In this study, we analyzed keloid tissue characteristics using HE staining and immunohistochemistry, revealing abnormal expression of FoxC1 and Notch3 in keloids. Lentiviral modulation of FoxC1 and Notch3 demonstrated that they promote the expression of α-SMA, fibronectin, collagen I, and Hes-1, enhancing the proliferation, migration, invasion, and cytokine production of keloid fibroblasts (KFs) while inhibiting apoptosis. Co-immunoprecipitation (CO-IP), dual-luciferase reporter assays, and chromatin immunoprecipitation (ChIP) confirmed that FoxC1 can directly bind to the Notch3 promoter and enhance its transcription. Additionally, in vivo, overexpression of FoxC1 and Notch3 promoted keloid formation. In summary, our research highlights the critical regulatory role of FoxC1 in keloid formation through Notch3 activation, potentially offering new therapeutic targets for preventing scar formation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114402"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of METTL3 in the proliferation, invasion, and migration of intrahepatic cholangiocarcinoma cells via m6A modification","authors":"Xinmiao Jiang ,&nbsp;Hui Tan","doi":"10.1016/j.yexcr.2024.114353","DOIUrl":"10.1016/j.yexcr.2024.114353","url":null,"abstract":"<div><div>Intrahepatic cholangiocarcinoma (ICC) is a primary invasive malignant tumor. This study was conducted to explore the role of methyltransferase-like 3 (METTL3)-mediated m6A modification in ICC cells and provide novel targets for ICC treatment. Levels of METTL3/YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)/Nedd4 family interacting protein 1 (NDFIP1) in cells were determined. Cell viability, proliferation, invasion, and migration were evaluated. The enrichments of METTL3, YTHDF2, and m6A on NDFIP1 mRNA were analyzed. The mRNA stability was determined. Inhibition of YTHDF2 or NDFIP1 was combined with si-METTL3 to confirm the mechanism. The role of METTL3 <em>in vivo</em> was verified. METTL3 was overexpressed in ICC cells. METTL3 silencing suppressed ICC cell malignant behaviors, which were reversed by METTL3 overexpression. METTL3 increased m6A modification on NDFIP1 mRNA, facilitated YTHDF2 recognition of m6A, and promoted NDFIP1 mRNA degradation, thereby suppressing NDFIP1 expression. YTHDF2 inhibition increased NDFIP1 mRNA levels. NDFIP1 downregulation partially reversed the inhibitory effects of si-METTL3 on ICC cell behaviors, while NDFIP1 overexpression partially reversed the promotive effects of METTL3 on ICC cell behaviors. METTL3 downregulation suppressed ICC growth by increasing NDFIP1 expression. In conclusion, METTL3 aggravates ICC cell proliferation, invasion, and migration by promoting the degradation of NDFIP1 mRNA in a YTHDF2-dependent manner.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114353"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The aberrantly activated AURKB supports and complements the function of AURKA in CALR mutated cells through regulating the cell growth and differentiation","authors":"Xueting Hu ,&nbsp;Xiangru Yu ,&nbsp;Liwei Zhang ,&nbsp;Qigang Zhang ,&nbsp;Mengchu Ji ,&nbsp;Kunming Qi ,&nbsp;Shujin Wang ,&nbsp;Zhenyu Li ,&nbsp;Kailin Xu ,&nbsp;Chunling Fu","doi":"10.1016/j.yexcr.2024.114377","DOIUrl":"10.1016/j.yexcr.2024.114377","url":null,"abstract":"<div><div>Aurora kinase B (AURKB) was reported to assist Aurora kinase A (AURKA) to regulate cellular mitosis. AURKA has been found activated in myeloproliferative neoplasms (MPNs) patients with CALR gene mutation, however, it's unclear whether AURKB displays a compensatory function of AURKA in regulation of CALR mutant cell growth and differentiation. Here, we found that AURKB, similar with AURKA, was aberrantly activated in CALR mutant patients, and displayed a more tolerance to the aurora kinase inhibitor. Inhibition of AURKA decreased cell growth and colony formation, induced cell differentiation and apoptosis, while, this inhibitive degree was further enhanced when AURKB was blocked by incremental inhibitor. Transcriptomic analyses revealed a more significant gene enrichment in cells with knockdown of AURKB than that of AURKA, mainly reflecting in oxidative phosphorylation, mitosis, proliferation and apoptosis signaling pathway. Moreover, downregulation of AURKB enhanced cell growth arrest and apoptosis more obviously than that of AURKA, and additionally promoted cell differentiation and metabolism-oxygen consumption rate (OCR). Otherwise, overexpression of AURKA or AURKB facilitated the cell proliferation of CALR mutant cells, and made cells more sensitive to the aurora kinase inhibitor. These results suggest that activated AURKB not only supports the functions of AURKA in promoting the growth of CALR mutated cells, but also has impeded the differentiation of these cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114377"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delactylation diminished the growth inhibitory role of CA3 by restoring DUOX2 expression in hepatocellular carcinoma","authors":"Jun Yan ,&nbsp;Yunfei Zhou ,&nbsp;Jianwen Xu ,&nbsp;Yihong Dong ,&nbsp;Xun Yang ,&nbsp;Xinxin Yang ,&nbsp;Aodi Wu ,&nbsp;Shuyuan Chang ,&nbsp;Yumeng Wang ,&nbsp;Qingxin Zhang ,&nbsp;Tomii Ayaka ,&nbsp;Lei Yu ,&nbsp;Liuyang Zhao ,&nbsp;Hongxue Meng ,&nbsp;Dabin Liu","doi":"10.1016/j.yexcr.2024.114392","DOIUrl":"10.1016/j.yexcr.2024.114392","url":null,"abstract":"<div><div>Lactylation is an emerging pathogenesis of hepatocellular carcinoma (HCC). However, the underlying mechanisms and biological significance remain poorly understood. The Carbonic anhydrase III (CA3) gene, previously defined as a binding protein of SQLE and involved in the NAFLD disease, has now been identified as a novel tumor suppressor in HCC. mRNA expression of CA3 is associated with a favorable prognosis and negatively correlated with serum lactate levels, whereas CA3 protein expression does not correlate with patient prognosis or serum lactate levels, suggested there has lactate-related post-translational modification of CA3 in HCC. Overexpression of CA3 induces cell apoptosis, thereby reducing intracellular reactive oxygen stress (ROS) through the inhibition of DUOX2 expression. The decreased lactylation level of CA3 protein at the K36 residues, induced by SQLE, results in the loss of the anti-cancer effect of CA3. Together, this study has demonstrated that CA3 is a novel tumor suppressor in HCC, and delactylation of CA3 represents a newly identified mechanism by which HCC cells evade growth suppressors.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114392"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the mechanism of microRNA-134 in colon cancer progression: Targeting KRAS and PIK3CA for cell cycle control and histone deacetylase regulation","authors":"Ganesan Jothimani ,&nbsp;Diptimayee Das ,&nbsp;Surajit Pathak ,&nbsp;Sarubala Malayaperumal ,&nbsp;Hong Zhang ,&nbsp;Xiao-Feng Sun ,&nbsp;Antara Banerjee","doi":"10.1016/j.yexcr.2024.114385","DOIUrl":"10.1016/j.yexcr.2024.114385","url":null,"abstract":"<div><div>Colon cancer is the leading cause of cancer-related deaths worldwide. MicroRNAs (miRNAs) are key regulators of gene expression, often dysregulated in colon cancer. This study aims to elucidate the therapeutic role of <em>miR-134-5p</em> as a tumor suppressor miRNA in colon cancer cells. We analyzed miRNA expression profiles in primary and metastatic colon cancer cells. The clinical significance of <em>miR-134-5p</em> was evaluated using the TCGA database. Bioinformatics tools (HADDOCK) predicted miRNA-mRNA interactions and the molecular docking of miRNA-mRNA-AGO2 complexes. Luciferase reporter assays, cell proliferation, immunofluorescence, colony forming unit assays, and qRT-PCR analysis assessed <em>miR-134-5p</em> effects on <em>KRAS</em>, <em>PIK3CA</em>, and downstream signaling pathways in primary and metastatic colon cancer cells. <em>miR-134-5p</em> was downregulated in colon cancer cells. Bioinformatics analysis suggested KRAS, <em>PIK3CA</em>, <em>EGFR</em>, and <em>HDAC5</em> as potential targets. HADDOCK analysis revealed strong binding affinity and structural stability between <em>KRAS</em>, <em>PIK3CA</em>, <em>miR-134-5p</em>, and AGO2. Gene-reporter assays confirmed <em>miR-134-5p</em>-mediated degradation of <em>KRAS</em> and <em>PIK3CA</em>. <em>miR-134-5p</em> transfection reduced <em>KRAS</em> and <em>PI3K</em> protein levels, suppressed <em>EGFR/RTK</em> signaling and its downstream targets, and inhibited HDAC expression, ultimately reducing colon cancer cell proliferation. The results of this study confirm that <em>miR-134-5p</em> acts as a potential tumor suppressor miRNA in colon cancer cells by inhibiting <em>KRAS</em> and <em>PI3K</em> expression through AGO2-mediated gene silencing. It deregulates downstream <em>EGFR</em> signaling and <em>HDACs</em>, thereby reducing colon cancer cell proliferation. These findings highlight <em>miR-134-5p</em> as a promising therapeutic target for miRNA-mediated anticancer therapy.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114385"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT3 mitigates high glucose-induced damage in retinal microvascular endothelial cells via OPA1-mediated mitochondrial dynamics","authors":"Jiemei Shi ,&nbsp;Min Liu ,&nbsp;Haohao Zhu ,&nbsp;Chunhui Jiang","doi":"10.1016/j.yexcr.2024.114320","DOIUrl":"10.1016/j.yexcr.2024.114320","url":null,"abstract":"<div><div>Oxidative stress in endothelial cells is pivotal in diabetic retinopathy (DR), with mitochondrial homeostasis being crucial to mitigate this stress. This study explored the roles of mitochondrial sirtuins (SIRTs) in high glucose (HG)-induced oxidative stress, related endothelial impairment, and mitochondrial homeostasis damage in rat retinal microvascular endothelial cells (RMECs). RMECs were cultured under HG or equivalent osmotic conditions. Cell viability was assessed using the Cell Counting Kit-8 assay, whereas cell death and survival were determined via calcein-AM/propidium iodide double staining. Reactive oxygen species (ROS) levels were measured using 2′,7′-dichlorofluorescein fluorescence. Expression of mitochondrial SIRTs3-5 and key mitochondrial homeostasis molecules was quantified by the quantitative real-time polymerase chain reaction and confirmed by western blotting. Mitochondrial morphology was evaluated using electron microscopy and the MitoTracker fluorescent probe. A SIRT3-overexpressing RMEC line was constructed to assess the role of SIRT3 in oxidative stress and mitochondrial dynamics. After 48 h of HG exposure, cell viability was significantly reduced, with a concomitant increase in cell death and ROS levels, alongside a marked decrease in SIRT3 expression and molecules associated with mitochondrial dynamics. SIRT3 overexpression reversed these effects, particularly increasing the mitochondrial fusion-related molecule, optic atrophy 1 (OPA1). However, the OPA1 inhibitor, MYLS22, blocked the protective effect of SIRT3, leading to more dead cells, a higher ROS level, and intensified mitochondrial fragmentation. These results suggest that SIRT3 is involved in HG-induced imbalanced mitochondrial dynamics of endothelial cells in DR, potentially through the OPA1 pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 2","pages":"Article 114320"},"PeriodicalIF":3.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142566340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}