Acta biochimica et biophysica Sinica最新文献_第4页

Succinate accumulation induces pyroptosis and mitochondrial damage via the inhibition of ATP5F1D in HUVECs. 琥珀酸积累通过抑制HUVECs中的ATP5F1D诱导热亡和线粒体损伤。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-15 DOI: 10.3724/abbs.2025116

Hong Huang, Jian Cui, Dan Tang, Xing Xiang, Jie Mao, Zhe He, Hengjing Hu, Zhangxiu He, Lu He, Huifang Tang

{"title":"Succinate accumulation induces pyroptosis and mitochondrial damage via the inhibition of ATP5F1D in HUVECs.","authors":"Hong Huang, Jian Cui, Dan Tang, Xing Xiang, Jie Mao, Zhe He, Hengjing Hu, Zhangxiu He, Lu He, Huifang Tang","doi":"10.3724/abbs.2025116","DOIUrl":"https://doi.org/10.3724/abbs.2025116","url":null,"abstract":"Atherosclerosis, a chronic inflammatory disorder, is pathophysiologically linked to endothelial cell (EC) pyroptosis. This study aims to elucidate the mechanisms by which succinate exacerbates EC pyroptosis through mitochondrial damage. Serum samples are collected from patients with coronary heart disease (CHD) and healthy controls (HCs), and the levels of succinate, interleukin (IL)-6, and IL-18 are quantified. To establish a succinate accumulation model, human umbilical vein endothelial cells (HUVECs) are treated with diethyl butyl malonate (DEBM), followed by analysis of inflammatory cytokines. The expression of pyroptosis-related proteins is assessed via western blot analysis. Morphological changes in pyroptotic vesicles and membrane pores are examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The mitochondrial membrane potential and reactive oxygen species (ROS) levels are evaluated via a JC-1 kit and MitoSOX, respectively. RNA sequencing (RNA-seq) is performed to identify potential target genes and regulatory pathways. To investigate the functional role of ATP5F1D, small interfering RNAs (siRNAs) are used to knockdown ATP5F1D, while lentiviral vectors are used to overexpress ATP5F1D in HUVECs. The results reveal significantly elevated levels of succinate, IL-6, and IL-18 in both CHD patients and DEBM-treated HUVECs. Succinate accumulation induced by DEBM triggers pyroptosis and mitochondrial damage in HUVECs, as evidenced by the upregulation of pyroptosis-related proteins and the impairment of mitochondrial structure and function. RNA sequencing analysis identifies ATP5F1D as a key downstream target of succinate accumulation. Downregulation of ATP5F1D promotes pyroptosis and mitochondrial injury in HUVECs, whereas restoration of ATP5F1D expression effectively mitigates these detrimental effects. Succinate-induced downregulation of ATP5F1D drives mitochondrial dysfunction and pyroptosis in HUVECs.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144858786","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

Unveiling the multifaceted roles of extracellular vesicles in cancer: insights from molecular imaging and engineering strategies. 揭示细胞外囊泡在癌症中的多方面作用：来自分子成像和工程策略的见解。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-08 DOI: 10.3724/abbs.2025123

Yuqin Teng, Gang Huang, Hao Yang

{"title":"Unveiling the multifaceted roles of extracellular vesicles in cancer: insights from molecular imaging and engineering strategies.","authors":"Yuqin Teng, Gang Huang, Hao Yang","doi":"10.3724/abbs.2025123","DOIUrl":"https://doi.org/10.3724/abbs.2025123","url":null,"abstract":"Extracellular vesicles (EVs), a class of nanoscale, membrane-bound vesicles secreted by various cell types, have emerged as rapidly advancing fields of research in recent years. This heterogeneous vesicle is a versatile carrier system for a variety of biomolecules, including proteins, nucleic acids, and metabolites. EVs play pivotal roles in intercellular communication, immune regulation, and disease pathogenesis, with particular implications for cancer biology. On the one hand, EVs promote tumor progression and metastasis by facilitating communication between cancer cells and their microenvironment. On the other hand, EVs carry noncoding RNAs, such as miRNAs and other regulatory RNAs, which directly modulate immune cell function or exert antitumor effects by influencing cancer cell proliferation and apoptosis. In addition to their biological roles, EVs show great potential as drug delivery systems because of their ability to be effectively taken up by target cells and stably deliver therapeutic payloads. In the context of cancer therapy, natural EVs demonstrate inherent therapeutic potential, particularly in targeting highly metabolically active organs. Furthermore, engineered EVs, which serve as both therapeutic vehicles and molecular imaging probes, have demonstrated significant potential for cancer theranostics. This review focuses on elucidating the dynamic changes and biological functions of EVs in vivo, with the aim of exploring the translational potential of EV-based molecular imaging and tracing technologies in cancer treatment. This work seeks to provide critical insights that may enhance the precision and efficacy of tumor therapies, offering a foundation for future clinical applications.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803245","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 TCF7L2/miR-206/Cofilin1 axis promotes the metastasis of bladder cancer cells by regulating the formation of invadopodia. TCF7L2/miR-206/Cofilin1轴通过调控侵足形成促进膀胱癌细胞转移。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-06 DOI: 10.3724/abbs.2025114

Yuzhen Jie, Yinggui Yang, Chengyan Guo, Qinghui Wu, Zhewen Ou, Weifu Wang, Ning Xu, Wei Peng, Yingguang Wu, Jiangfan Peng, Shengchao Ma, Shufang Zhang, Fei Wang

{"title":"The TCF7L2/miR-206/Cofilin1 axis promotes the metastasis of bladder cancer cells by regulating the formation of invadopodia.","authors":"Yuzhen Jie, Yinggui Yang, Chengyan Guo, Qinghui Wu, Zhewen Ou, Weifu Wang, Ning Xu, Wei Peng, Yingguang Wu, Jiangfan Peng, Shengchao Ma, Shufang Zhang, Fei Wang","doi":"10.3724/abbs.2025114","DOIUrl":"https://doi.org/10.3724/abbs.2025114","url":null,"abstract":"Bladder cancer (BCa) is one of the most common malignant tumors of the urinary system, but its pathogenesis is still unclear. T1G3 BCa is particularly invasive and relapses readily after treatment, with progression to invasive cancer or distant metastasis. Therefore, identification of the molecular mechanism by which it invades and metastasizes to guide treatment and predict patient prognosis is needed. Cofilin1 plays an important role in regulating gene expression and the invasiveness of tumors. In this study, we show that Cofilin1 is highly expressed in BCa and lymph nodes with metastasis, which is positively related to the grade of BCa, and is significantly related to clinicopathological parameters and cancer-specific survival. Phenotypic analysis reveals that Cofilin1 knockout inhibits the proliferation and migration of BCa cells, whereas Cofilin1 overexpression promotes the opposite phenotype. Cofilin1 binds to cortactin, thereby reducing the expression of F-actin and promoting the formation of invadopodia in BCa cells. Further experiments reveal that TCF7L2 can bind to the promoter of Cofilin1 and transactivate it, promoting a malignant phenotype. TCF7L2 may also reverse the inhibitory effect of miR-206 on the binding of Cofilin1 and cortactin and promote the metastasis of BCa by inhibiting the transcription maturation of miR-206. This study confirms that Cofilin1 is an oncogene in T1G3 BCa, and the TCF7L2/miR-206/Cofilin1 signaling pathway plays an important role in the formation of invadopodia in BCa.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144797935","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

TMEM16A inhibition suppresses melanoma metastasis. TMEM16A抑制抑制黑色素瘤转移。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-05 DOI: 10.3724/abbs.2025133

Na Zhou, Chuangxin Pei, Xue Lu, Peng Shi, Siqi Wu, Huaqun Chen

引用次数: 0

IKZF3 promotes gastric cancer progression via Hedgehog signaling activation and is targetable by SANT-1. IKZF3通过Hedgehog信号激活促进胃癌进展，并可被st -1靶向。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-04 DOI: 10.3724/abbs.2025103

Muhammad Ali, Shantanu Baral, Jun Ren, Liuhua Wang, Bin Liu, Sen Wang, Daorong Wang

{"title":"IKZF3 promotes gastric cancer progression via Hedgehog signaling activation and is targetable by SANT-1.","authors":"Muhammad Ali, Shantanu Baral, Jun Ren, Liuhua Wang, Bin Liu, Sen Wang, Daorong Wang","doi":"10.3724/abbs.2025103","DOIUrl":"https://doi.org/10.3724/abbs.2025103","url":null,"abstract":"Elevated expression of Aiolos family zinc finger 3 (IKZF3), a transcription factor crucial for lymphocyte maturation, is observed in hematological cancers. However, its role in gastric cancer (GC) remains unclear. We detect the increased IKZF3 levels in GC tissues using immunohistochemical, qRT-PCR and western blot analysis. The function of IKZF3 in GC cells is further studied through CCK-8, Transwell, colony formation, scratch wound healing, and flow cytometry assays. IKZF3 overexpression significantly promotes GC cell invasion, migration, and proliferation, whereas IKZF3 knockdown induces cell cycle arrest at the G1/S phase. Flow cytometry confirms these alterations in cell cycle dynamics. Using the JASPAR database, we determine that IKZF3 binds to the SMO promoter region, thereby activating SMO expression. Notably, the SMO inhibitor SANT-1 effectively reverses IKZF3-mediated effects. Furthermore, IKZF3 promotes GC tumor growth in xenograft models. Our findings highlight the pivotal role of IKZF3 in GC progression by modulating SMO expression and activating the Hedgehog signaling pathway. Therapeutically, targeting IKZF3 with SANT-1 is promising for mitigating GC proliferation and invasion. This study provides insights into potential therapeutic approaches targeting IKZF3 for GC treatment.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783193","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

Construction of an ASFV proteome library via multiple optimization strategies for high-throughput analysis. 基于多种优化策略的非洲猪瘟蛋白质组文库构建及高通量分析。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-01 DOI: 10.3724/abbs.2025125

Songxin Guo, Li Ouyang, Hui Zhang, Ming Li, Wei Zhou, Ao Liang, Lu Wang, Rui Gong, Dianbing Wang, Chenli Liu, Zhuojun Dai, Shengce Tao, Jiaoyu Deng, Guimin Zhang, Xian-En Zhang, Feng Li

{"title":"Construction of an ASFV proteome library via multiple optimization strategies for high-throughput analysis.","authors":"Songxin Guo, Li Ouyang, Hui Zhang, Ming Li, Wei Zhou, Ao Liang, Lu Wang, Rui Gong, Dianbing Wang, Chenli Liu, Zhuojun Dai, Shengce Tao, Jiaoyu Deng, Guimin Zhang, Xian-En Zhang, Feng Li","doi":"10.3724/abbs.2025125","DOIUrl":"https://doi.org/10.3724/abbs.2025125","url":null,"abstract":"African swine fever virus (ASFV) is a large and structurally complex DNA virus encoding more than 160 proteins, including more than 68 structural proteins. A protein library covering recombinant ASFV proteins is fundamentally important for studies on protein function, antigenicity, vaccine development, and virus-host interactions. Here, to construct an ASFV protein library, we add a glutathione S-transferase (GST) tag at the N-terminus of each ASFV protein to facilitate solubilization and purification and express the recombinant proteins in the yeast host. By optimizing codons, expression vectors and strains and conditions of expression and purification, we achieve satisfactory protein yields for analytical applications and maximized access to the whole proteome of ASFV, with coverage of ca. 95%. Using the library, a protein chip is constructed and used to screen for interactions between ASFV and swine proteins (e.g., IRF3, p65, and IκBα). The ASFV protein library lays the groundwork for understanding and combatting ASFV. The methods for constructing the library are instructive for generating other protein libraries for high-throughput applications.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758876","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

Nanchangmycin suppresses influenza A virus infection by blocking endosomal acidification. 南昌霉素通过阻断内体酸化抑制甲型流感病毒感染。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-08-01 DOI: 10.3724/abbs.2025102

Hao Zhang, Changhai Liu, Shuo Cai, Yuting Wu, Lu Shang, Fayu Yang, Jing Liu, Nan Wei, Yingchun Liu, Mi Wang, Fei Gao, Qinfang Liu, Hongjun Chen, Guangzhi Tong, Yin Chen, Feng Gu

{"title":"Nanchangmycin suppresses influenza A virus infection by blocking endosomal acidification.","authors":"Hao Zhang, Changhai Liu, Shuo Cai, Yuting Wu, Lu Shang, Fayu Yang, Jing Liu, Nan Wei, Yingchun Liu, Mi Wang, Fei Gao, Qinfang Liu, Hongjun Chen, Guangzhi Tong, Yin Chen, Feng Gu","doi":"10.3724/abbs.2025102","DOIUrl":"https://doi.org/10.3724/abbs.2025102","url":null,"abstract":"Influenza A viruses (IAVs) constitute a major threat to human and animal health. Currently, M2 ion-channel inhibitors, neuraminidase (NA) inhibitors, RNA polymerase inhibitors, and cap-dependent endonuclease inhibitors have been applied clinically as therapeutics against IAVs. However, IAVs possess adaptive mutations to these inhibitors, especially M2 ion channel and NA inhibitors. Thus, novel antiviral agents should be developed. In the present study, we screen approximately 5500 compounds and identify an IAV inhibitor, nanchangmycin, which possesses a robust antiviral activity both in vitro and in vivo. In addition, it exhibits broad-spectrum antiviral activity for additional virus infections, including pseudorabies virus, herpes virus, porcine epidemic diarrhea virus, porcine reproductive and respiratory syndrome virus. Most importantly, it has antiviral activity against oseltamivir-resistant strains in sub-μM ranges and promotes the survival of MDCK cells infected with the oseltamivir-resistant influenza A virus strain. Further studies reveal that it blocks the nuclei migration of viral nuclear proteins (NPs), resulting in NP accumulation in the cytoplasm, particularly within perinuclear endosomes. Also, it inhibits IAVs by blocking endosomal acidification. Overall, nanchangmycin has the potential to be developed as an anti-influenza agent.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758877","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

NLRP3 inflammasome activity and pyroptosis are involved in CD206 ⁺ macrophage activation by MPO anti-neutrophil cytoplasmic antibodies. NLRP3炎性体活性和焦亡参与了MPO抗中性粒细胞胞浆抗体活化CD206 +巨噬细胞。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-07-30 DOI: 10.3724/abbs.2025080

Zhaonan Wei, Xiaoning An, Yinyin Xie, Yan Shen, Liyan Ni, Jing Xu, Yimei Wang, Pingyan Shen, Hao Shi, Wen Zhang, Yongxi Chen

{"title":"NLRP3 inflammasome activity and pyroptosis are involved in CD206 + macrophage activation by MPO anti-neutrophil cytoplasmic antibodies.","authors":"Zhaonan Wei, Xiaoning An, Yinyin Xie, Yan Shen, Liyan Ni, Jing Xu, Yimei Wang, Pingyan Shen, Hao Shi, Wen Zhang, Yongxi Chen","doi":"10.3724/abbs.2025080","DOIUrl":"https://doi.org/10.3724/abbs.2025080","url":null,"abstract":"Macrophages are key players in the pathology of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Existing studies and our previous studies have documented the role of CD206-positive M2 macrophages in the inflammatory process of AAV. Inflammasome activation is a critical pathway through which macrophages release inflammatory factors. In this study, we investigate the role of the inflammasome in macrophages in AAV and explore the role of CD206 in this process. We recruit newly diagnosed AAV patients and disease controls from our department. The expression and localization of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) and CD206 in the kidney are determined via immunofluorescence experiments. Myeloperoxidase (MPO)-ANCA immunoglobulin G (MPO-ANCA IgG) is purified from new-onset AAV patients with MPO-ANCA and used to treat lipopolysaccharide (LPS)-primed macrophages in vitro. Our findings reveal that NLRP3 expression is significantly elevated in the kidneys of active AAV patients, accompanied by increased cleaved caspase-1 and N-terminal gasdermin-D (GSDMD) levels in peripheral blood mononuclear cells (PBMCs). In vitro, MPO-ANCA IgG induces NLRP3 inflammasome activation and interleukin (IL)-1β production in macrophages, which is associated with increased MPO expression and JNK signaling pathway activation. Immunofluorescence analysis demonstrates partial colocalization of CD206 and NLRP3 in AAV kidneys. Furthermore, silencing of MRC1 gene, which encodes CD206, reduces inflammasome activation induced by MPO-ANCA IgG. In conclusion, our study provides evidence that MPO-ANCA IgG contributes to NLRP3 inflammasome activation and macrophage pyroptosis, with CD206 playing a critical role in this process. These findings elucidate the mechanisms underlying inflammation in AAV and suggest potential therapeutic targets.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740815","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

METTL3-mediated m ⁶A modification facilitates Nectin-4-induced VNN1 upregulation and promotion of ESCC progression. mettl3介导的m6a修饰促进nectin -4诱导的VNN1上调和促进ESCC进展。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-07-30 DOI: 10.3724/abbs.2025108

Yuanfeng Long, Hang Yang, Ruolan Zhang, Quanneng Zhao, Mi Yang, Guiqin Song, Kang Liu

{"title":"METTL3-mediated m 6A modification facilitates Nectin-4-induced VNN1 upregulation and promotion of ESCC progression.","authors":"Yuanfeng Long, Hang Yang, Ruolan Zhang, Quanneng Zhao, Mi Yang, Guiqin Song, Kang Liu","doi":"10.3724/abbs.2025108","DOIUrl":"https://doi.org/10.3724/abbs.2025108","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. N6-methyladenosine (m 6A) RNA modification plays a role in tumorigenesis, but its contributions to ESCC and the regulation of cell adhesion molecules such as Nectin-4 are not fully elucidated. In this study, we investigate the role and the regulatory mechanisms of Nectin-4 in ESCC, particularly regarding the influence of m 6A modification and its downstream metabolic effects. Our study demonstrates that methyltransferase-like protein 3 (METTL3) enhances Nectin-4 mRNA stability and expression through m 6A methylation in ESCC, as validated by actinomycin D assay, MeRIP-qPCR, and dual-luciferase reporter assay. Both METTL3 and Nectin-4 are highly expressed in ESCC tissues and promote malignant phenotypes such as proliferation, migration, and invasion. Further analysis identifies pantothenate esterase 1 (VNN1) as a downstream target of Nectin-4, mediating the oncogenic effects of the METTL3/Nectin-4 axis and promoting the biosynthesis of pantothenic acid and coenzyme A, thus driving ESCC progression. By integrating transcriptomic data, this study elucidates a key pathogenic mechanism in which the METTL3/Nectin-4/VNN1 axis regulates metabolic reprogramming to promote ESCC development. These findings provide new insights into the molecular pathology of ESCC and offer potential biomarkers and therapeutic targets for early screening, prognosis, and precision treatment for ESSC.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752030","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

CDR1as modulates arrhythmia post-myocardial infarction via regulating Cav1.2. CDR1as通过调节Cav1.2调控心肌梗死后心律失常。

IF 3.4 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-07-29 DOI: 10.3724/abbs.2025126

Jiapan Wang, Wenjie Liao, Xingda Li, Zhen Chen, Chunlei Duan, Zhenru Wang, Hongda Li, Haonan Du, Ye Yuan, Zhimin Du

{"title":"CDR1as modulates arrhythmia post-myocardial infarction via regulating Cav1.2.","authors":"Jiapan Wang, Wenjie Liao, Xingda Li, Zhen Chen, Chunlei Duan, Zhenru Wang, Hongda Li, Haonan Du, Ye Yuan, Zhimin Du","doi":"10.3724/abbs.2025126","DOIUrl":"https://doi.org/10.3724/abbs.2025126","url":null,"abstract":"Arrhythmias, especially ventricular arrhythmias (VAs), are the primary cause of mortality following myocardial infarction (MI) and are typically attributable to electrophysiological disorders of the heart. Our previous work demonstrated that CDR1as knockdown ameliorates arrhythmias by modulating Nav1.5 and Kir6.2 channels post-MI. This study aims to explore the role of CDR1as in calcium channel remodeling subsequent to ischemic arrhythmia. We employ MI in mice by ligating the left anterior descending coronary artery (LAD) and use patch-clamp techniques to measure the Ca current ( I CaL) in isolated ventricular cardiomyocytes. The results show that the expression of Cav1.2 is significantly decreased in the infarct border zone at 12 h post-MI. CDR1as knockdown via AAV9-CDR1as-shRNA administration leads to an enhancement of cardiac function and a restoration of both I CaL density and Cav1.2 expression in MI model mice. These findings indicate that targeting the CDR1as pathway to modulate calcium channels can be a viable strategy for antiarrhythmic therapy following MI.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740814","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