Cell Cycle最新文献_第4页

An updated view on lagging strand DNA replication: implications for the replication stress response. 后链DNA复制的最新观点：对复制应激反应的影响。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-03-22 DOI: 10.1080/15384101.2026.2646889

Rodrigo Martín-Rufo, Emilio Lecona

{"title":"An updated view on lagging strand DNA replication: implications for the replication stress response.","authors":"Rodrigo Martín-Rufo, Emilio Lecona","doi":"10.1080/15384101.2026.2646889","DOIUrl":"10.1080/15384101.2026.2646889","url":null,"abstract":"The process of DNA replication is inherently asymmetric. While the leading strand is synthesized continuously, the lagging strand is copied in small fragments, the Okazaki fragments, requiring the repeated priming by the DNA polymerase alpha/Primase complex (Pol α/Pri). Current evidence is consistent with a semi-distributive model for priming in the lagging strand, as Pol α/Pri acts associated to the replisome and also as a free complex. In addition, there is a strong link between the dynamics of replication in the lagging strand and the basal activation of the replication stress response (RSR) during an unperturbed S phase. We hypothesize that the RSR monitors the generation of Okazaki fragments to control the synthesis of DNA in what we call the DNA replication control (DRC) mode of the RSR. The DRC enforces a gradual progression of DNA replication by restricting origin firing, what is necessary to establish the replication program in the cell and to prevent the appearance of genomic instability. Thus, the RSR coordinates the replication program in the cell, modulating the progression of DNA replication to prevent the exhaustion of cellular resources that would endanger the stability of the genome.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-16"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13007448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493814","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}

引用次数: 0

Metformin counteracts lipid accumulation and cell proliferation in hepatocellular carcinoma via regulating METTL3-mediated m⁶A methylation. 二甲双胍通过调节mettl3介导的m6A甲基化来对抗肝细胞癌的脂质积累和细胞增殖。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-05-03 DOI: 10.1080/15384101.2026.2665248

Yannan Qi, Chuanrui Chen, Yuwei Dai, Zhouyuan Wang, Xinyi Liu, Chenxi Guo, Meina Wang, Zhigang Hu, Hongjie Di

{"title":"Metformin counteracts lipid accumulation and cell proliferation in hepatocellular carcinoma via regulating METTL3-mediated m6A methylation.","authors":"Yannan Qi, Chuanrui Chen, Yuwei Dai, Zhouyuan Wang, Xinyi Liu, Chenxi Guo, Meina Wang, Zhigang Hu, Hongjie Di","doi":"10.1080/15384101.2026.2665248","DOIUrl":"https://doi.org/10.1080/15384101.2026.2665248","url":null,"abstract":"Metformin, a first-line antidiabetic drug, has demonstrated anticancer potential in various malignancies, yet its precise mechanisms in hepatocellular carcinoma (HCC) remain incompletely defined. Here, we show that metformin inhibits lipid accumulation and proliferation in HCC cells through modulation of N6-methyladenosine (m6A) RNA methylation. Treatment of HepG2 and Huh7 cells with metformin significantly reduced intracellular triglyceride and cholesterol levels, concomitant with decreased lipid droplet accumulation and impaired cell proliferation. Mechanistically, metformin lowered global m6A methylation by downregulating the m6A methyltransferase Methyltransferase-like 3 (METTL3), while upregulating the demethylase Fat mass and obesity-associated protein (FTO). Functional assays revealed that METTL3 overexpression restored lipid accumulation and proliferation in metformin-treated cells, whereas METTL3 knockdown phenocopied the lipid-lowering and anti-proliferative effects of metformin. Further analyses identified the METTL3/ACC1/FASN axis as a critical downstream pathway, with metformin suppressing m6A modification and expression of Fatty acid synthase (FASN) and Acetyl-CoA carboxylase 1 (ACC1) transcripts - effects reversed by METTL3 overexpression. These findings establish METTL3 as a central mediator of metformin's metabolic and antiproliferative activities in HCC, uncovering a previously unappreciated epitranscriptomic mechanism by which metformin impedes tumor progression.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-15"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811693","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}

引用次数: 0

Repurposing the anti-gout drug benzbromarone for the treatment of glioma. 将抗痛风药物苯溴马龙用于治疗神经胶质瘤。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-11-07 DOI: 10.1080/15384101.2025.2587234

Mengmeng Huo, Ziwei Wang, Wanying Guo, Jun Gong, Helin Lu, Wu Liu, Liqiong Ding

{"title":"Repurposing the anti-gout drug benzbromarone for the treatment of glioma.","authors":"Mengmeng Huo, Ziwei Wang, Wanying Guo, Jun Gong, Helin Lu, Wu Liu, Liqiong Ding","doi":"10.1080/15384101.2025.2587234","DOIUrl":"10.1080/15384101.2025.2587234","url":null,"abstract":"Glioma has long been a threat to human health and new treatments are required to address this health problem. We here explored the potential use of benzbromarone as a supplement to existing chemotherapy strategies. The effects of benzbromarone on the proliferation and migration of C6 glioma cells were evaluated by MTT and wound healing assays. The effects of benzbromarone on cell cycle arrest and apoptosis in C6 glioma cells were determined by flow cytometry. The effect of benzbromarone on reactive oxygen species (ROS) production was determined through fluorescence microscopy and flow cytometry. Finally, the effect of benzbromarone on the NF-κB pathway was determined by western blotting and immunofluorescence. Benzbromarone inhibited the growth and migration of C6 glioma cells in a concentration-dependent manner. Benzbromarone also induced cell cycle arrest and apoptosis in C6 glioma cells, in addition to increasing ROS generation. Western blot analysis revealed that benzbromarone activated the NF-κB signaling pathway. Our results suggest that benzbromarone induces cytotoxicity through ROS production. These findings indicate the potential of benzbromarone as a treatment of glioma.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-12"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457705","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}

引用次数: 0

Targeting IMPDH to inhibit SAMHD1 in KMT2A-rearranged leukaemia. 靶向IMPDH抑制kmt2a重排白血病中的SAMHD1。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-12-15 DOI: 10.1080/15384101.2025.2601796

Yolande Klootsema, Nikolaos Tsesmetzis, Sushma Sharma, Sophia Hofmann, Jonas Thier, Christopher Dirks, Femke M Hormann, Miriam Yagüe-Capilla, Anna Bohlin, Sofia Bengtzen, Sören Lehmann, Andrei Chabes, Martin Jädersten, Vanessa Lundin, Sean G Rudd, Ingrid Lilienthal, Nikolas Herold

{"title":"Targeting IMPDH to inhibit SAMHD1 in KMT2A-rearranged leukaemia.","authors":"Yolande Klootsema, Nikolaos Tsesmetzis, Sushma Sharma, Sophia Hofmann, Jonas Thier, Christopher Dirks, Femke M Hormann, Miriam Yagüe-Capilla, Anna Bohlin, Sofia Bengtzen, Sören Lehmann, Andrei Chabes, Martin Jädersten, Vanessa Lundin, Sean G Rudd, Ingrid Lilienthal, Nikolas Herold","doi":"10.1080/15384101.2025.2601796","DOIUrl":"10.1080/15384101.2025.2601796","url":null,"abstract":"Cytarabine (ara-C) and fludarabine (F-ara-A) are key drugs in leukaemia treatment. SAMHD1 is known to confer resistance to ara-C and F-ara-A, and we previously identified ribonucleotide reductase inhibitors as indirect SAMHD1 inhibitors in a phenotypic screen. The inosine monophosphate dehydrogenase (IMPDH) inhibitor mycophenolic acid (MPA) was also a hit in this screen. IMPDH inhibitors (IMPDHi) have previously shown efficacy against KMT2A-rearranged (KMT2Ar) acute myeloid leukaemia (AML). We investigated whether IMPDH inhibition could enhance the effect of ara-C and F-ara-A in AML cell lines and primary AML samples, and whether this effect was linked to KMT2A status. We found that sensitivity to IMPDHi was independent of KMT2A status. IMPDHi synergized with ara-C and F-ara-A in a SAMHD1-dependent manner in a subset of AML cells, but not in acute lymphoblastic leukaemia cell lines. Mechanistically, IMPDHi depleted allosteric SAMHD1 activators GTP and dGTP, thereby increasing active triphosphate metabolites in SAMHD1-proficient, but not SAMHD1-deficient, cells. Our findings suggest that the addition of IMPDHi to ara-C and F-ara-A may have therapeutic benefits in some AML cases.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-19"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145762405","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}

引用次数: 0

CTDSPL2 facilitates resistance to paclitaxel in breast cancer cells by suppressing SCYL1 phosphorylation. CTDSPL2通过抑制SCYL1磷酸化促进乳腺癌细胞对紫杉醇的抗性。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-04-27 DOI: 10.1080/15384101.2026.2663187

Jing Zhao, Wei Zhao, Zhimin Wei, Feng Hou, Lingling Sun, Xia Li, Xianning Dong

{"title":"CTDSPL2 facilitates resistance to paclitaxel in breast cancer cells by suppressing SCYL1 phosphorylation.","authors":"Jing Zhao, Wei Zhao, Zhimin Wei, Feng Hou, Lingling Sun, Xia Li, Xianning Dong","doi":"10.1080/15384101.2026.2663187","DOIUrl":"https://doi.org/10.1080/15384101.2026.2663187","url":null,"abstract":"Breast cancer (BC) exhibits significant heterogeneity and complexity and is leading causes of mortality in women globally. Paclitaxel (PTX) is commonly utilized as the primary medication for BC. However, the resistance of BC to PTX poses a significant challenge in clinical treatment. This study aimed at to explore whether carboxy-terminal domain small phosphatase like 2 (CTDSPL2) affected PTX resistance in BC cells. PTX resistant BC cell lines, including MCF-7/PTX and MDA-MB-231/PTX, were developed by continuously increasing PTX concentration, and we found that CTDSPL2 was upregulated in BC cells with PTX resistance. Loss-of-function studies showed that CTDSPL2 knockdown caused a decrease in cytotoxicity and proliferative ability in PTX-resistant BC cells, as well as enhanced cell apoptotic rate and DNA damage. The results from nanoparticle tracking analysis (NTA) indicated that CTDSPL2 knockdown also suppressed the secretion of extracellular vesicles. In vivo tumorigenesis assays showed that CTDSPL2 downregulation inhibited tumorigenicity of nude mice injecting with PTX-resistant BC cells. Co-immunoprecipitation (Co-IP) assay demonstrated the binding between CTDSPL2 and SCY1-like pseudokinase 1 (SCYL1). The increased level of SCYL1 phosphorylation evoked by CTDSPL2 knockdown in PTX-resistant cancer cells was blocked after mutating the serine 754 site of SCYL1 to alanine. In conclusion, the present study identifies CTDSPL2 as a new factor in BC that plays an essential role in PTX-resistant BC cells through the regulation of SCYL1 phosphorylation.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-18"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13123077/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763433","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}

引用次数: 0

MicroRNAs in chemotherapy-induced peripheral neuropathy: mechanisms and therapies. 化疗诱导的周围神经病变中的microrna：机制和治疗。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2025-12-09 DOI: 10.1080/15384101.2025.2600440

Sepide Javankiani, Faeze Dehghani, Foroozan Yarahmadi, Arian Jahandideh, Fatemeh Asadi, Moein Ghasemi, Danial Akhondi, Zohal Nasiri, Vahid Zarrintan, Mahtab Moradian, Kaveh Mehrvar, Farzad Salmannezhad Khorami, Qumars Behfar

{"title":"MicroRNAs in chemotherapy-induced peripheral neuropathy: mechanisms and therapies.","authors":"Sepide Javankiani, Faeze Dehghani, Foroozan Yarahmadi, Arian Jahandideh, Fatemeh Asadi, Moein Ghasemi, Danial Akhondi, Zohal Nasiri, Vahid Zarrintan, Mahtab Moradian, Kaveh Mehrvar, Farzad Salmannezhad Khorami, Qumars Behfar","doi":"10.1080/15384101.2025.2600440","DOIUrl":"10.1080/15384101.2025.2600440","url":null,"abstract":"Chemotherapy-induced peripheral neuropathy (CIPN) is a significant adverse effect of cancer therapies that profoundly disrupts the quality of life for patients. CIPN is characterized by sensory symptoms such as pain, tingling, and numbness, typically distributed in a \"glove and stocking\" pattern. Its underlying mechanisms remain incompletely understood, involving complex processes such as heightened neuronal excitability, alterations in ion channel function, neuroinflammation, and glial cell activation. MicroRNAs (miRNAs), small non-coding RNA molecules, play a pivotal role in regulating these processes by modulating gene expression and cellular functions. Emerging evidence suggests that specific miRNAs, including miR-30b-5p, miR-155, miR-124, and miR-21, are involved in regulating pathways that contribute to CIPN-related pain. These miRNAs influence the function of ion channels, glial cell activation, and neuroinflammation. MiRNAs hold significant promise as biomarkers for the early detection of CIPN. This review comprehensively examines the current understanding of miRNA-mediated mechanisms contributing to CIPN development. Key miRNAs implicated in modulating these pathways are discussed in detail, including their potential as diagnostic biomarkers and therapeutic targets. By integrating molecular insights with translational approaches, this review provides a framework for future research and clinical applications targeting miRNA pathways to mitigate CIPN and improve outcomes for cancer patients undergoing chemotherapy.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"1-17"},"PeriodicalIF":3.4,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145707475","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}

引用次数: 0

Statement of Retraction: A novel role for fanconi anemia (FA) pathway effector protein FANCD2 in cell cycle progression of untransformed primary human cells. 撤销声明：范可尼贫血（FA）通路效应蛋白FANCD2在未转化的原代人细胞周期进程中的新作用。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2026-02-26 DOI: 10.1080/15384101.2026.2624973

引用次数: 0

Enigmatic functions of ATP8B1: cholestasis, inflammation, phosphoinositide flipping, and cellular homeostasis. ATP8B1的神秘功能：胆汁淤积、炎症、磷酸肌肽翻转和细胞内稳态。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-14 DOI: 10.1080/15384101.2025.2574275

Ashutosh Prince, C Alicia Traughber, Yavar Shiravand, Nilam Bhandari, Mariam R Khan, Swati Sharma, Kara Timinski, Karen F Murray, Laura N Bull, Kailash Gulshan

{"title":"Enigmatic functions of ATP8B1: cholestasis, inflammation, phosphoinositide flipping, and cellular homeostasis.","authors":"Ashutosh Prince, C Alicia Traughber, Yavar Shiravand, Nilam Bhandari, Mariam R Khan, Swati Sharma, Kara Timinski, Karen F Murray, Laura N Bull, Kailash Gulshan","doi":"10.1080/15384101.2025.2574275","DOIUrl":"10.1080/15384101.2025.2574275","url":null,"abstract":"Mutations in ATP8B1 cause a spectrum of cholestatic liver disease, ranging from Progressive-Familial-Intrahepatic-Cholestasis type-1 (PFIC1) to Benign-Recurrent-Intrahepatic-Cholestasis type-1 (BRIC1). Manifestations of PFIC1 include severe pruritus, jaundice, and liver damage. Extrahepatic features sometimes observed in PFIC1 include sensorineural hearing loss, diarrhea, pancreatitis, and short stature. ATP8B1 was shown to translocate phospholipids across the plasma membrane; however, expression of ATP8B1 in many tissues and the range of pathological manifestations in ATP8B1 deficiency suggest diverse physiological functions of ATP8B1, and pleiotropic mechanisms regulating its activity. Recent studies suggest that phosphoinositides, including PIP2 and PIP3, can function as regulators, substrates, and binding partners of ATP8B1. New research shows that ATP8B1 modulates host immune system by regulating cleavage of pyroptotic-executioner Gasdermin D (GSDMD), and inflammation-resolution pathways such as phagocytosis/efferocytosis. Further mechanistic insights can accelerate development of new therapies for restoring membrane integrity, reducing inflammasome activity, and correcting metabolic imbalances caused by ATP8B1 dysfunction.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"409-421"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285728","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}

引用次数: 0

The GABBR1/miR-19b-3p/WNT2B axis regulates insulin resistance and liver injury in diabetes with viral infection: mechanistic and therapeutic insights. GABBR1/miR-19b-3p/WNT2B轴调节病毒感染糖尿病的胰岛素抵抗和肝损伤：机制和治疗见解

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-09-25 DOI: 10.1080/15384101.2025.2564744

Rui Yang, Jiangling Zhu, Lin Zou, Yingxuan Li, Li Peng, Xing Wang, Qian Xi, Fei Sun, Junhua Ma, Xia Chen

{"title":"The GABBR1/miR-19b-3p/WNT2B axis regulates insulin resistance and liver injury in diabetes with viral infection: mechanistic and therapeutic insights.","authors":"Rui Yang, Jiangling Zhu, Lin Zou, Yingxuan Li, Li Peng, Xing Wang, Qian Xi, Fei Sun, Junhua Ma, Xia Chen","doi":"10.1080/15384101.2025.2564744","DOIUrl":"10.1080/15384101.2025.2564744","url":null,"abstract":"Insulin resistance (IR) is the main feature of type 2 diabetes mellitus. Furthermore, viral infection can aggravate the abnormal glucose metabolism in diabetic patients. GABBR1 can maintain normal glucose homeostasis, but its specific role in diabetes is not clear. We investigated the function of the GABBR1/miR-19b-3p/WNT2B axis in vitro and in vivo. miR-19b-3p and GABBR1 were overexpressed or knocked down in AML12 cells. Subsequently, these cells were treated with palmitic acid (PA) to induce damage or poly I : C to mimic viral infection. The degree of AML12 cell damage was assessed using the CCK-8 assay; inflammation levels were measured using ELISA; and IR indexes were determined using the Immunofluorescence kit and Western blot assay. The diabetic mice model was established to evaluate liver injury and IR. PA and poly I : C can reduce the activity of AML12 cells, increase apoptosis and inflammatory factor contents, weaken the ability of glucose uptake and consumption, enhance the production capacity, and reduce the level of GLUT4. GABBR1 mediates the targeted regulation of WNT2B by miR-19b-3p. PA and poly I : C also increased ALT, AST, inflammatory factors and miR-19b-3p levels, and decreased GABBR1 and WNT2B expression of mice. Liver cells showed swelling and many spherical lipid droplets. After miR-19b-3p knockdown and GABBR1 overexpression, the degree of liver injury and IR in AML12 cells and mice were alleviated. GABBR1 regulates miR-19b-3p/WNT2B axis to reduce liver injury, IR and inflammatory response, and improve the comorbidity of diabetes and viral infection. This pathway represents a potential therapeutic target for mitigating the comorbidity of diabetes and viral infection.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"566-585"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147837","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}

引用次数: 0

HSP22 reduces diabetic cardiomyopathy by inhibition oxidative stress and inflammation. HSP22通过抑制氧化应激和炎症降低糖尿病性心肌病。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-04 DOI: 10.1080/15384101.2025.2581629

Lingling Yu, Shengsong Chen, Weifang Zhang, Chahua Huang, Longlong Hu, Liang Liu, Yun Yu, Qian Liang, Huihui Bao, Xiaoshu Cheng

{"title":"HSP22 reduces diabetic cardiomyopathy by inhibition oxidative stress and inflammation.","authors":"Lingling Yu, Shengsong Chen, Weifang Zhang, Chahua Huang, Longlong Hu, Liang Liu, Yun Yu, Qian Liang, Huihui Bao, Xiaoshu Cheng","doi":"10.1080/15384101.2025.2581629","DOIUrl":"10.1080/15384101.2025.2581629","url":null,"abstract":"Heat shock protein 22 (HSP22) can reduce type 2 diabetes mellitus (T2DM) induced vascular endothelial injury by inhibition of inflammation and oxidative stress. Therefore, we explored whether HSP22 alleviated diabetes cardiomyopathy (DCM) in mice. A T2DM mouse model was constructed and myocardial tissues were used to perform transcriptome sequencing. HSP22 transgenic and HSP22 knockout mice were established to confirm its role in DCM. Transthoracic echocardiography, hematoxylin-eosin staining, TUNEL staining and apoptosis-related proteins were detected to evaluate myocardial injury. Dihydroethidium staining, malondialdehyde and superoxide dismutase levels were detected to evaluate myocardial oxidative stress. We performed RT-PCR to detect inflammatory factors and evaluate the myocardial inflammatory response. Immunohistochemical staining, RT-PCR and western blot were used to define the expression of HSP22 in mouse myocardial tissues. Transcriptome sequencing analysis revealed the expression of HSP22 in myocardium of T2DM mice significantly decreases. GO analysis found that oxidative stress and inflammatory response were closely related to DCM in mice. Furthermore, HSP22 overexpression can alleviate DCM in mice and HSP22 knockout aggravated DCM. HSP22 reduced oxidative stress and inflammation to alleviate DCM in mice.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"655-669"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145437481","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}

引用次数: 0