Apoptosis最新文献_第7页

Exosome-mediated triple drug delivery enhances apoptosis in pancreatic cancer cells 外泌体介导的三重药物递送促进胰腺癌细胞凋亡。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-06-09 DOI: 10.1007/s10495-025-02131-y

Ruixia Zhang, Yongjie Zhang, Fei Hao, Zhengxing Su, Xing Duan, Xiangrong Song

{"title":"Exosome-mediated triple drug delivery enhances apoptosis in pancreatic cancer cells","authors":"Ruixia Zhang, Yongjie Zhang, Fei Hao, Zhengxing Su, Xing Duan, Xiangrong Song","doi":"10.1007/s10495-025-02131-y","DOIUrl":"10.1007/s10495-025-02131-y","url":null,"abstract":"<div><p>Pancreatic cancer (PC) is one of the most common malignant tumors of the digestive tract. Gemcitabine (GEM) is a first-line chemotherapeutic agent for unresectable PC, but systemic distribution of the drug, drug resistance, and clinical side effects undermine its efficacy. This study utilized bone marrow mesenchymal stem cell-derived exosomes (BMSC-EXOs) as a delivery vehicle for a triple-drug combination (galectin-9 siRNA/DOGEM/indocyanine green) to improve synergistic therapy against PC. Galectin-9 siRNA, prodrug DOGEM, and ICG were loaded into BMSC-Exos by electroporation and vortexing to prepare nanoformulations (iEXO-DG-ICG). iEXO-DG-ICG had an average size of 132 ± 2.6 nm and its release rate in pH 6.0 medium was all faster than in pH 7.4 medium. The cytotoxicity of iEXO-DG-ICG against PANC-02 cells was stronger than free GEM both in vitro and in vivo. The protein expression of galectin-9 in tumor cells decreased by 79% after treatment with iEXO-DG-ICG, and the proportions of CD8⁺ T cells and IFN-γ⁺ CD8⁺ T cells increased while the proportions of Tregs decreased. The tumor inhibition rate of iEXO-DG-ICG was 90.3%. The present study successfully constructed a multimodal delivery system, designated iEXO-DG-ICG, using EXO derived from BM-MSCs as carriers. This system exhibited good tumor targeting and pH-responsive release characteristics. Both in vitro and in vivo studies confirmed that iEXO-DG-ICG significantly enhanced anti-tumor effects through the synergistic effect of chemotherapy, immunotherapy, and phototherapy. These findings provide a new strategy and a research foundation for the clinical treatment of pancreatic cancer.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1893 - 1911"},"PeriodicalIF":8.1,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246094","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}

引用次数: 0

The mechanistic study of quercetin in the treatment of alcoholic brain injury via the JNK/P38 MAPK signaling pathway 槲皮素通过JNK/P38 MAPK信号通路治疗酒精性脑损伤的机制研究

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-06-02 DOI: 10.1007/s10495-025-02125-w

Yang Zhang, Binchuan Wang, Lisha Liu, Xu Huang, Yu Cai, Lishang Liao, Xuefeng Min, Yingjiang Gu

{"title":"The mechanistic study of quercetin in the treatment of alcoholic brain injury via the JNK/P38 MAPK signaling pathway","authors":"Yang Zhang, Binchuan Wang, Lisha Liu, Xu Huang, Yu Cai, Lishang Liao, Xuefeng Min, Yingjiang Gu","doi":"10.1007/s10495-025-02125-w","DOIUrl":"10.1007/s10495-025-02125-w","url":null,"abstract":"<div><p>Alcoholic brain damage (ABD) stems from chronic excessive alcohol consumption, causing neuroinflammation, oxidative stress, mitochondrial dysfunction, and neuronal apoptosis, all of which severely impair cognition and quality of life. However, traditional treatments have shown limited efficacy. Quercetin (QE), a natural flavonoid with antioxidant, anti-inflammatory, and neuroprotective properties, may therefore offer a promising approach for ABD. Accordingly, this study examines QE’s potential mechanisms, with an emphasis on its modulation of the JNK/P38 MAPK pathway. In vitro, QE’s effects on BV2 and HT22 cell viability were assessed via the CCK8 assay. Additionally, oxidative stress markers, including reactive oxygen species (ROS) and glutathione, were measured. Transmission electron microscopy was employed to observe cellular changes, while flow cytometry was used to evaluate apoptosis. Furthermore, western blotting was conducted to analyze the expression of BAX, Bcl-2, Caspase-3, IL-1, IL-6, TNF-α, P-P38, P-JNK, P38, and JNK. In vivo, SD rats were divided into a control group, an ethanol group, and three QE groups (25, 50, 100 mg/kg body weight), which were treated concurrently with ethanol for 12 weeks. Behavioral tests, histological staining, oxidative stress markers, and protein expression were examined. QE increased superoxide dismutase (SOD) activity, lowered ROS and malondialdehyde (MDA) levels, and reduced mitochondrial damage in vitro. It also significantly inhibited ethanol-induced apoptosis, inflammation, and JNK/P38 MAPK activation. Furthermore, QE improved spatial cognition, reduced anxiety, and ameliorated oxidative and inflammatory damage. Overall, QE alleviated alcohol-induced neuronal injury by suppressing oxidative stress, apoptosis, and inflammation via the JNK/P38 MAPK pathway, highlighting its therapeutic potential for ABD.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1875 - 1892"},"PeriodicalIF":8.1,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207496","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}

引用次数: 0

Polymeric immunoglobulin receptor (pIgR) in cancer progression: a critical role and potential therapeutic target 聚合免疫球蛋白受体（pIgR）在癌症进展中的关键作用和潜在的治疗靶点。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-26 DOI: 10.1007/s10495-025-02116-x

Shaoju Qian, Yeqing He, Ruixue Li, Panpan Sun, Xingyi Zhang, Lin Pan, Zhishan Xu, Zhiwei Feng, Rong Lian, Lili Yu

{"title":"Polymeric immunoglobulin receptor (pIgR) in cancer progression: a critical role and potential therapeutic target","authors":"Shaoju Qian, Yeqing He, Ruixue Li, Panpan Sun, Xingyi Zhang, Lin Pan, Zhishan Xu, Zhiwei Feng, Rong Lian, Lili Yu","doi":"10.1007/s10495-025-02116-x","DOIUrl":"10.1007/s10495-025-02116-x","url":null,"abstract":"<div><p>Polymeric immunoglobulin receptor (pIgR) is a crucial receptor that primarily mediates the transcytosis of immunoglobulins A and M across epithelial cells, emerging as an essential participant in modulating both mucosal immunity and innate immunity. Recently, pIgR dysregulation in cancer has garnered widespread attention. It exhibits distinct mechanisms and effects across various cancer types with significant clinical value as a biomarker for malignant tumor diagnosis and prognosis evaluation. Recent therapeutic advances have revealed promising strategies, including dimeric IgA-based approaches targeting intracellular oncogenic drivers through pIgR-mediated transcytosis, small molecule modulators such as bufalin, and targeting EV-pIgR with neutralizing antibodies. Integrating these approaches with conventional therapies presents opportunities for enhanced treatment efficacy. Specifically, blocking EV-pIgR with neutralizing antibodies, when integrated with conventional hepatocellular carcinoma therapies such as sorafenib or other therapeutic agents, or a dIgA-targeting approach combined with immune checkpoint inhibitors, may enhance treatment efficacy. This review also addresses current challenges and future directions in pIgR-targeted cancer therapy, emphasizing the need for a deeper understanding of pIgR's regulatory mechanisms. These insights reveal that pIgR is an emerging therapeutic target with significant potential for the development of novel cancer treatment strategies.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1751 - 1775"},"PeriodicalIF":8.1,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144140979","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}

引用次数: 0

Retraction Note: The microtubule depolymerizing agent naphthazarin induces both apoptosis and autophagy in A549 lung cancer cells 注：微管解聚剂萘萨林可诱导A549肺癌细胞凋亡和自噬。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-19 DOI: 10.1007/s10495-025-02124-x

Bipul R. Acharya, Surela Bhattacharyya, Diptiman Choudhury, Gopal Chakrabarti

引用次数: 0

ω-6 PUFA-enriched membrane phospholipid composition of cardiomyocytes increases the susceptibility to iron-induced ferroptosis and inflammation ω-6 pufa富集的心肌细胞膜磷脂组成增加了铁诱导的铁下垂和炎症的易感性。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-17 DOI: 10.1007/s10495-025-02121-0

Sungji Cho, Eddie Tam, Khang Nguyen, Yubin Lei, Carine Fillebeen, Kostas Pantopoulos, Hye Kyoung Sung, Gary Sweeney

{"title":"ω-6 PUFA-enriched membrane phospholipid composition of cardiomyocytes increases the susceptibility to iron-induced ferroptosis and inflammation","authors":"Sungji Cho, Eddie Tam, Khang Nguyen, Yubin Lei, Carine Fillebeen, Kostas Pantopoulos, Hye Kyoung Sung, Gary Sweeney","doi":"10.1007/s10495-025-02121-0","DOIUrl":"10.1007/s10495-025-02121-0","url":null,"abstract":"<div><p>Ferroptosis is an attractive therapeutic target in cardiometabolic disease (CMD); however, its contribution to myocardial damage requires further elucidation. This study was designed to examine whether altered phospholipid composition in cardiomyocytes enhanced ferroptosis susceptibility, and the underlying mechanisms. Human iPSC-derived cardiomyocytes and H9c2 cells were used to study iron-induced lipid peroxidation, cell death, and inflammation after exposure to different types of fatty acids. Lipidomic analysis was performed using LC/MS to assess changes in phospholipid composition, with a focus on ω-6 PUFA-containing phospholipids. Cellular and mitochondrial lipid peroxidation, sterile inflammation, and cell death were evaluated. Additionally, the release of damage-associated molecular patterns (DAMPs) and macrophage responses, including STING and type I interferon (IFN-I) signaling, were investigated. LC/MS lipidomic analysis indicated that treating cells with arachidonic acid (AA) elevated ω-6 PUFA-containing phospholipids, particularly phosphatidylethanolamines (PE) and phosphatidylcholines (PC). This significantly increased susceptibility to iron-induced total cellular as well as mitochondrial lipid peroxidation. Subsequently, increased release of mitochondrial DNA to cytosol was detected, resulting in both sterile inflammation and subsequent cell death. Furthermore, iron-induced release of one or more damage associated molecular patterns (DAMP) from AA-treated cells that induced crosstalk with macrophages eliciting a STING and type I interferon (IFN-I) response. These results indicate that cardiomyocytes enriched with ω-6 PUFA-containing phospholipids are more susceptible to lipid peroxidation, underscoring ferroptosis as a critical factor in myocardial damage associated with CMD.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 5-6","pages":"1614 - 1627"},"PeriodicalIF":8.1,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085672","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}

引用次数: 0

GJB2 as a novel prognostic biomarker associated with immune infiltration and cuproptosis in ovarian cancer GJB2作为一种新的与卵巢癌免疫浸润和铜增生相关的预后生物标志物。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-15 DOI: 10.1007/s10495-025-02119-8

Han Lei, Ke Guo, Guang Shu, Maonan Wang, Yu Li, Zhihui Tan, Qiong Pan, Gang Yin

{"title":"GJB2 as a novel prognostic biomarker associated with immune infiltration and cuproptosis in ovarian cancer","authors":"Han Lei, Ke Guo, Guang Shu, Maonan Wang, Yu Li, Zhihui Tan, Qiong Pan, Gang Yin","doi":"10.1007/s10495-025-02119-8","DOIUrl":"10.1007/s10495-025-02119-8","url":null,"abstract":"<div><p>Cuproptosis, a recently identified copper-dependent cell death mechanism, remains poorly unexplored in ovarian cancer (OC). This study systematically evaluates clinically significant cuproptosis-related genes (CRGs) as potential prognostic biomarkers in OC. Cox regression analysis and LASSO algorithms were used to develop a prognostic risk model incorporating 5 CRGs (<i>CD8B2</i>, <i>GJB2</i>, <i>GRIP2</i>, <i>MELK</i>, and <i>PLA2G2D</i>) within the TCGA cohort. This model stratified OC patients into high-risk and low-risk groups, with the high-risk group exhibiting significantly shorter overall survival compared to the low-risk group. The model's predictive accuracy for prognosis in OC patients was validated in the TCGA training cohort, TCGA testing cohort, and ICGC external validation cohorts. Among these 5 signature genes, the number of cuproptosis genes associated with <i>GJB2</i> is the largest, so we selected <i>GJB2</i> for further validation. qPCR revealed that <i>GJB2</i> was highly expressed in OC cells and tumor tissues. The high expression of <i>GJB2</i> was closely associated with poor prognosis in OC patients. Functionally, <i>GJB2</i> silencing suppressed OC cell proliferation and migration while its overexpression promoted malignant progression and EMT. Furthermore, <i>GJB2</i> regulated copper homeostasis and reduced cuproptosis sensitivity, while also facilitating immune escape by inhibiting CD8<sup>+</sup> T cell infiltration and cytokine secretion, revealing its multiple roles in OC progression. In conclusion, we established a novel prognostic model incorporating 5 CRGs that effectively predicts clinical outcomes and characterizes the immune microenvironment in OC. Our findings particularly highlight <i>GJB2</i> as a key regulator of cuproptosis with significant potential as both a prognostic biomarker and therapeutic target for OC management.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 5-6","pages":"1589 - 1613"},"PeriodicalIF":8.1,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12167356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075482","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}

引用次数: 0

Diallyl disulfide in oncotherapy: molecular mechanisms and therapeutic potentials 二烯丙基二硫在肿瘤治疗中的作用：分子机制和治疗潜力。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-15 DOI: 10.1007/s10495-025-02105-0

Yun-Fei Zhou, Yi-Wen Zhu, Yan-Wen Wang, Xiao-Yi Liang, Qi-Ying Jiang, Dong-Dong Wu

{"title":"Diallyl disulfide in oncotherapy: molecular mechanisms and therapeutic potentials","authors":"Yun-Fei Zhou, Yi-Wen Zhu, Yan-Wen Wang, Xiao-Yi Liang, Qi-Ying Jiang, Dong-Dong Wu","doi":"10.1007/s10495-025-02105-0","DOIUrl":"10.1007/s10495-025-02105-0","url":null,"abstract":"<div><p>Garlic possesses a broad spectrum of medicinal properties, such as anti-cancer, antioxidant, anti-diabetic effects, and protective effects on the heart, nervous system, and liver. Diallyl disulfide (DADS), an oil-soluble organic sulfur-containing compound in garlic, has garnered attention in recent years for its demonstrated anti-cancer efficacy in various cancer types such as leukemia, breast cancer, hepatocellular carcinoma, stomach cancer, and prostate cancer. The anticancer properties of DADS are attributed to its ability to suppress cancer cell proliferation, impede invasion and metastasis, as well as induce apoptosis, promote differentiation, and facilitate cell cycle arrest. Although many literatures have reviewed the pharmacokinetics, molecular mechanisms of anti-cancer effects and some clinical trials of DADS, the specific mechanisms and clinical-translational therapeutic potentials have not been elucidated. This comprehensive review focuses on delineating the molecular mechanisms underlying the anticancer effects of DADS, with a particular emphasis on its potential utility as a therapeutic intervention in the clinical management of cancer, and analyzes the challenges and coping strategies faced in the application of DADS as an anti-cancer drug, pointing out the directions for scientific research.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1730 - 1750"},"PeriodicalIF":8.1,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075480","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}

引用次数: 0

Tumor heterogeneity and resistance in glioblastoma: the role of stem cells 胶质母细胞瘤的肿瘤异质性和耐药性：干细胞的作用。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-15 DOI: 10.1007/s10495-025-02123-y

Nikita Ghosh, Debarpan Chatterjee, Aparna Datta

{"title":"Tumor heterogeneity and resistance in glioblastoma: the role of stem cells","authors":"Nikita Ghosh, Debarpan Chatterjee, Aparna Datta","doi":"10.1007/s10495-025-02123-y","DOIUrl":"10.1007/s10495-025-02123-y","url":null,"abstract":"<div><p>Glioblastoma multiforme (GBM) is one of the most aggressive and treatment-resistant brain tumor, characterized by its heterogeneity and the presence of glioblastoma stem cells (GSCs). GSCs are a subpopulation of cells within the tumor that possess self-renewal and differentiation capabilities, contributing to tumor initiation, progression, and recurrence. This review explores the unique biological properties of GSCs, including their molecular markers, signalling pathways, and interactions with the tumor microenvironment. We discuss the mechanisms by which GSCs evade conventional therapies, such as enhanced DNA repair and metabolic plasticity, which complicate treatment outcomes. Furthermore, we highlight recent advancements in identifying novel biomarkers and therapeutic targets that may improve the efficacy of treatments aimed at GSCs. The potential of targeted therapies, including immunotherapy and combination strategies, is also examined to overcome the challenges posed by GSCs. Ultimately, a deeper understanding of GSC biology is essential for developing personalized treatment approaches that can enhance patient outcomes in glioblastoma.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 7-8","pages":"1695 - 1729"},"PeriodicalIF":8.1,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075484","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}

引用次数: 0

Inhibition of SIRT1/HSF1 pathway contributes to doxorubicin-induced nephrotoxicity in ovarian tumor-bearing mice 抑制SIRT1/HSF1通路有助于阿霉素诱导的卵巢荷瘤小鼠肾毒性。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-10 DOI: 10.1007/s10495-025-02122-z

Mo Chen, Ying Zhao, Song Hu, Jun-bo Yuan, Kang-jie Xie, Shu-nv Cai, Xiao-yan Zhu, Jian-kui Du, Ping-bo Xu

{"title":"Inhibition of SIRT1/HSF1 pathway contributes to doxorubicin-induced nephrotoxicity in ovarian tumor-bearing mice","authors":"Mo Chen, Ying Zhao, Song Hu, Jun-bo Yuan, Kang-jie Xie, Shu-nv Cai, Xiao-yan Zhu, Jian-kui Du, Ping-bo Xu","doi":"10.1007/s10495-025-02122-z","DOIUrl":"10.1007/s10495-025-02122-z","url":null,"abstract":"<div><p>Doxorubicin (DOX) is a common drug used in chemotherapy to treat for advanced ovarian cancer, but it can cause organ damage, particularly to the kidneys. This study aimed to investigate whether the SIRT1/HSF1 pathway is associated with DOX-induced nephrotoxicity. Bioinformatics analysis was performed using single-cell RNA sequencing (scRNA-seq) data from DOX-treated kidneys to investigate the potential mechanism of DOX-induced renal damage. To explore the role of HSF1 in DOX-induced nephrotoxicity, the lentivirus HSF1 (Lv-HSF1) was injected after tumor implantation, followed by DOX administration. DOX prevented ovarian tumor growth but caused renal injury in mice, as evidenced by elevated UACR, increased blood BUN levels, and abnormalities in kidney structure and fibrosis. Bioinformatic analysis revealed fewer podocytes in the kidneys of DOX-exposed mice than in those of control mice, which was further confirmed by examining renal tissue and murine podocyte cells. Gene set enrichment analysis revealed significant enrichment of HSF1-dependent transactivation and HSF1 activation pathways specifically within podocytes obtained from DOX-treated mice, which was also validated in renal tissue samples. Furthermore, HSF1A attenuated DOX-induced podocyte injury in vitro. Lv-HSF1-targeted podocytes mitigate DOX-induced podocyte injury in vivo. Notably, SIRT1 expression was significantly downregulated in both kidney tissues and podocytes subjected to DOX treatment. The observed damage to podocytes induced by DOX may be attributed to an increase in HSF1 acetylation facilitated through the downregulation of SIRT1, a process that can be counteracted by the administration of the SIRT1 agonist RSV. Collectively, these findings demonstrated that suppression of the SIRT1/HSF1 signaling pathway contributes to DOX-mediated nephrotoxicity in mice bearing ovarian tumors.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"30 5-6","pages":"1572 - 1588"},"PeriodicalIF":8.1,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967256","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}

引用次数: 0

Correction to: Elevated serum mtDNA in COVID‑19 patients is linked to SARS‑CoV‑2 envelope protein targeting mitochondrial VDAC1, inducing apoptosis and mtDNA release 更正：COVID - 19患者血清mtDNA升高与靶向线粒体VDAC1的SARS - CoV - 2包膜蛋白有关，可诱导细胞凋亡和mtDNA释放。

IF 8.1 2区生物学

Apoptosis Pub Date : 2025-05-10 DOI: 10.1007/s10495-025-02113-0

Anna Shteinfer‑Kuzmine, Ankit Verma, Rut Bornshten, Eli Ben Chetrit, Ami Ben‑Ya’acov, Hadas Pahima, Ethan Rubin, Yosef Mograbi, Eyal Shteyer, Varda Shoshan‑Barmatz

引用次数: 0