International journal of molecular medicine最新文献_第2页

Lipid metabolism in microglia: Emerging mechanisms and therapeutic opportunities for neurodegenerative diseases (Review). 小胶质细胞的脂质代谢：神经退行性疾病的新机制和治疗机会（综述）。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/ijmm.2025.5580

Yunlong Sun, Kaifang Wei, Xudong Liao, Jian'an Wang, Li'na Gao, Bo Pang

{"title":"Lipid metabolism in microglia: Emerging mechanisms and therapeutic opportunities for neurodegenerative diseases (Review).","authors":"Yunlong Sun, Kaifang Wei, Xudong Liao, Jian'an Wang, Li'na Gao, Bo Pang","doi":"10.3892/ijmm.2025.5580","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5580","url":null,"abstract":"Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis, are characterized by progressive neuronal loss and neuroinflammation, with microglial dysfunction emerging as a central driver of pathogenesis. Microglia, the central nervous system‑resident immune cells, exhibit dual pro‑inflammatory and anti‑inflammatory phenotypes, dynamically regulated by lipid metabolic reprogramming. Chronic activation of M1 microglia exacerbates neuronal damage, while M2 microglia promote tissue repair via phagocytic clearance and neurotrophic factor secretion. Lipid dysregulation‑marked by ceramide accumulation, cholesterol esterification defects and oxidized lipid‑driven neuroinflammation‑critically modulates microglial polarization. Mechanistic studies reveal that mitochondrial dysfunction, lysosomal stress and ferroptosis intersect with lipid metabolic pathways to amplify neurotoxicity. Therapeutic strategies targeting lipid homeostasis, such as TREM2 agonism, demonstrate efficacy in preclinical models by restoring microglial function and mitigating pathology. This review synthesizes emerging evidence linking microglial lipid metabolism to NDD progression, highlighting novel biomarkers and therapeutic avenues to disrupt the lipid‑neuroinflammation axis in neurodegeneration.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Integrated multi‑omics analysis of liver metabolic dysregulation in ACE2 knockout mice. ACE2敲除小鼠肝脏代谢失调的综合多组学分析。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-09-01 Epub Date: 2025-07-04 DOI: 10.3892/ijmm.2025.5575

Shuai Xiao, Jinxiu Guo, Bo Yu, Shiyuan Zhao, Yicun Shang, Ni Li, Jiyao Cui, Fangqiang Song, Pei Jiang

{"title":"Integrated multi‑omics analysis of liver metabolic dysregulation in ACE2 knockout mice.","authors":"Shuai Xiao, Jinxiu Guo, Bo Yu, Shiyuan Zhao, Yicun Shang, Ni Li, Jiyao Cui, Fangqiang Song, Pei Jiang","doi":"10.3892/ijmm.2025.5575","DOIUrl":"10.3892/ijmm.2025.5575","url":null,"abstract":"The present study systematically investigated the impact of angiotensin‑converting enzyme 2‑knockout (ACE2KO) on hepatic metabolic homeostasis and its molecular mechanisms using integrated transcriptomic, proteomic and metabolomic profiling. ACE2KO exacerbated hepatic lipid accumulation, as evidenced by elevated total cholesterol and triglyceride levels, while disrupting the renin‑angiotensin system equilibrium via increased angiotensin II levels and reduced angiotensin‑(1‑7) levels. Histopathological analysis revealed hepatocyte edema, vacuolar degeneration and inflammatory infiltration in the ACE2KO mice. Multi‑omics integration revealed systemic metabolic dysregulation. Transcriptomics identified 1,004 differentially expressed genes, including lipid metabolism regulators (Scd1 and Fabp1) and circadian rhythm modulators (Arntl and Cry1), proteomics identified 191 differentially expressed proteins associated with interferon signaling activation (Oas1a and Rsad2) and lipid synthesis suppression (Scd1 and Fasn), and metabolomics highlighted 193 differentially expressed metabolites indicative of bile acid dysregulation, glutathione redox imbalance and amino acid metabolism anomalies. Cross‑omics analysis indicated that ACE2 is a key regulator of metabolic homeostasis. Its absence causes systematic metabolic disorders, including lipid metabolism disorder, amino acid metabolic imbalance and detoxification dysfunction. These findings comprehensively delineated the multifaceted role of ACE2 in hepatic metabolic homeostasis, and provided mechanistic insights into and therapeutic targets for ACE2‑associated liver diseases.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TNF‑α induces premature senescence in tendon stem cells via the NF‑κB and p53/p21/cyclin E/CDK2 signaling pathways. TNF - α通过NF - κB和p53/p21/cyclin E/CDK2信号通路诱导肌腱干细胞过早衰老。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/ijmm.2025.5581

Hua Guo, Haixia Cao, Qian Lu, Zhifeng Gu, Guijuan Feng

{"title":"TNF‑α induces premature senescence in tendon stem cells via the NF‑κB and p53/p21/cyclin E/CDK2 signaling pathways.","authors":"Hua Guo, Haixia Cao, Qian Lu, Zhifeng Gu, Guijuan Feng","doi":"10.3892/ijmm.2025.5581","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5581","url":null,"abstract":"Achilles tendinitis (AT) is a complex disorder that affects tendon tissue and often responds poorly to non‑steroidal anti‑inflammatory drugs. Tumor necrosis factor‑α (TNF‑α), a proinflammatory cytokine involved in cell death and immune regulation, serves a central role in AT progression. The present study investigated the effects of TNF‑α on tendon stem cells (TSCs) and evaluated potential therapeutic strategies for AT. TNF‑α‑induced changes in TSCs were determined by investigating markers of cellular senescence, reactive oxygen species (ROS) activity, DNA damage and the expression of key transcription factors, including NF‑κB (phosphorylated‑p65, p65), p53, p21, cyclin E and CDK2. To determine whether TNF‑α‑induced senescence could be reversed, TSCs were treated with etanercept, a TNF‑α‑specific inhibitor. TNF‑α stimulation induced significant senescence in TSCs, as evidenced by increased ROS production, DNA damage and altered expression of senescence‑associated transcription factors. TNF‑α activated the NF‑κB and p53/p21/cyclin E/CDK2 signaling pathways, promoting TSC senescence. Etanercept treatment effectively reversed these effects, decreasing TSC senescence, suppressing inflammatory cell infiltration, decreasing TNF‑α protein expression and mitigating collagen fiber degradation. TNF‑α promotes TSCs senescence through specific signaling pathways and etanercept can counteract these deleterious effects. These results provide insights into the pathogenesis of AT and highlight TNF‑α inhibition as a promising therapeutic approach. Targeting TNF‑α may offer a novel treatment strategy for individuals with AT.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review). MEX3A在肿瘤发生中的作用：机制、肿瘤特异性效应和治疗意义（综述）。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/ijmm.2025.5579

Lulu Tang, Li Zhang, Shun Yao, Xin Li, Yongfeng Wang, Qian Liu, Jiajia Li, Guorong Wen, Jiaxing An, Hai Jin, Jiaxing Zhu, Biguang Tuo

{"title":"Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).","authors":"Lulu Tang, Li Zhang, Shun Yao, Xin Li, Yongfeng Wang, Qian Liu, Jiajia Li, Guorong Wen, Jiaxing An, Hai Jin, Jiaxing Zhu, Biguang Tuo","doi":"10.3892/ijmm.2025.5579","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5579","url":null,"abstract":"Muscle excess 3A (MEX3A), a dual‑function RNA‑binding protein with E3 ubiquitin ligase activity, is a pivotal regulator of tumorigenesis. By modulating mRNA stability, translation and targeted protein degradation, MEX3A orchestrates key oncogenic processes, including tumor stemness maintenance, proliferation, migration and immune evasion. MEX3A is aberrantly expressed in various malignancies, such as colorectal and breast cancer, hepatocellular carcinoma and glioblastoma, where it engages key signaling pathways, including the Wnt/β‑catenin, PI3K/AKT and NF‑κB pathways. Mechanistically, MEX3A directly regulates oncogenic and tumor suppressor transcripts, influencing the cell dynamics within the tumor microenvironment. Furthermore, MEX3A upregulation is associated with a poor prognosis and therapy resistance, highlighting its potential as a prognostic biomarker and therapeutic target. The present review aimed to summarize the molecular functions, tumor‑specific roles and translational relevance of MEX3A, bridging the gap between mechanistic insight and clinical applications. Future studies exploring MEX3A‑targeted interventions may reveal novel strategies for precision oncology.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lactate and lactylation in the kidneys: Current advances and prospects (Review). 肾脏乳酸和乳酸化：目前的进展和前景（综述）。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-08-01 Epub Date: 2025-06-06 DOI: 10.3892/ijmm.2025.5562

Xu Li, Lan Hu, Qin Hu, Hua Jin

引用次数: 0

Role and mechanisms of cuproptosis in the pathogenesis of Wilson's disease (Review). 铜突起在Wilson病发病机制中的作用和机制（综述）。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-08-01 Epub Date: 2025-06-06 DOI: 10.3892/ijmm.2025.5558

Hong Chen, Xie Wang, Jin Xing, Yue Pu, Hao Ye, Ying Ma, Juan Zhang

{"title":"Role and mechanisms of cuproptosis in the pathogenesis of Wilson's disease (Review).","authors":"Hong Chen, Xie Wang, Jin Xing, Yue Pu, Hao Ye, Ying Ma, Juan Zhang","doi":"10.3892/ijmm.2025.5558","DOIUrl":"10.3892/ijmm.2025.5558","url":null,"abstract":"Copper, an indispensable trace element in living organisms, plays a pivotal role in human physiological processes. Wilson's disease (WD), an inherited disorder of copper metabolism, is caused by mutations in the ATP7B gene. This genetic malfunction disrupts the dynamics of copper transport and metabolism, thereby impairing ceruloplasmin synthesis and copper excretion. The resultant accumulation of copper in various tissues and organs precipitates a cascade of cellular demise and functional impairment. Notably, cuproptosis, a recently discovered copper‑dependent regulated cell death mechanism, distinctly deviates from conventional cell death paradigms. This novel mode of cell death involves the interaction of copper with lipoacylated proteins within the tricarboxylic acid cycle, leading to proteinotoxic stress and culminating in cell death. In the realm of pathophysiology, cuproptosis has emerged as a pivotal player in a spectrum of diseases, with WD standing as a paradigm closely intertwined with the dysregulation of copper metabolism. This study aimed to encapsulate the pivotal molecular underpinnings of cuproptosis and delve into its crucial involvement in the etiopathogenesis of WD. By elucidating these mechanisms, the present analysis contributes significantly to the nuanced understanding of the pathological underpinnings of WD, thereby providing fresh insights and evidence that may direct innovative therapeutic strategies for this condition.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Corrigendum] miR‑335 promotes ferroptosis by targeting ferritin heavy chain 1 in in vivo and in vitro models of Parkinson's disease. [勘误]miR - 335在体内和体外帕金森病模型中通过靶向铁蛋白重链1促进铁下垂。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-08-01 Epub Date: 2025-06-13 DOI: 10.3892/ijmm.2025.5565

Xinrong Li, Wenwen Si, Zhan Li, Ye Tian, Xuelei Liu, Shanyu Ye, Zifeng Huang, Yichun Ji, Caiping Zhao, Xiaoqian Hao, Dongfeng Chen, Meiling Zhu

{"title":"[Corrigendum] miR‑335 promotes ferroptosis by targeting ferritin heavy chain 1 in in vivo and in vitro models of Parkinson's disease.","authors":"Xinrong Li, Wenwen Si, Zhan Li, Ye Tian, Xuelei Liu, Shanyu Ye, Zifeng Huang, Yichun Ji, Caiping Zhao, Xiaoqian Hao, Dongfeng Chen, Meiling Zhu","doi":"10.3892/ijmm.2025.5565","DOIUrl":"10.3892/ijmm.2025.5565","url":null,"abstract":"Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, for the JC‑1 staining experiments shown in Fig. 5F on p. 9, the 'mimic NC' and 'inhibitor' panels appeared to show the same cells, even though the green/red ratio was different comparing between the two data panels. In addition, two further instances of duplicated data panels were identified in Figs. S2 and S3, such that data that were allegedly obtained under different experimental conditions appeared to have been derived from the same original sources. After having asked the authors to explain the errors that had occurred in assembling these figures, they responded to explain that the error in Fig. 5F resulted from the incorrect selection of source images for the channels during the image merging process, whereas the errors in Figs. S2 and S3 occurred due to mistakes made in the naming and management of image files during storage. This led to the unintentional use of incorrect images during the process of figure assembly. Moreover, the authors were able to present to the Editorial Office the original data from the JC‑1 staining experiments belonging to Fig. 5F. The Editor of International Journal of Molecular Medicine has agreed that a corrigendum may be published to account for the errors made in assembling Figs. 5, S2 and S3, and the corrected versions of these figures are shown on the next page. All the authors agree with the publication of this corrigendum, and are thankful to the Editor for giving them the opportunity to present this; moreover, the Editor and the authors apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 47: 61, 2021; DOI: 10.3892/ijmm.2021.4894].","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lobetyolin alleviates IMQ‑induced psoriasis‑like skin inflammation by maintaining the homeostasis of the skin and inhibiting the inflammatory cytokines in dendritic cells. Lobetyolin通过维持皮肤稳态和抑制树突状细胞中的炎症因子来减轻IMQ诱导的牛皮癣样皮肤炎症。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-08-01 Epub Date: 2025-06-13 DOI: 10.3892/ijmm.2025.5563

Jianping He, Chenxi Feng, Yaohan Xu, Siji Chen, Jie Chen, Jingying Pan, Yinjing Song, Hao Cheng, Jiang Zhu, Jie Zhu

{"title":"Lobetyolin alleviates IMQ‑induced psoriasis‑like skin inflammation by maintaining the homeostasis of the skin and inhibiting the inflammatory cytokines in dendritic cells.","authors":"Jianping He, Chenxi Feng, Yaohan Xu, Siji Chen, Jie Chen, Jingying Pan, Yinjing Song, Hao Cheng, Jiang Zhu, Jie Zhu","doi":"10.3892/ijmm.2025.5563","DOIUrl":"10.3892/ijmm.2025.5563","url":null,"abstract":"Psoriasis, the most common inflammatory skin disease, is marked by excessive proliferation of keratinocytes and infiltration of immune cells into the epidermis. Current treatments, particularly biologics targeting the IL‑23/IL‑17 axis, demonstrate excellent efficacy, but issues of recurrence and side effects persist. Therefore, it is essential to identify safer and more effective alternatives. Lobetyolin (LBT), a key component of polyacetylenes in Codonopsis pilosula, exhibits potent antioxidant and antitumor properties, yet its potential for treating psoriasis remains unexplored. In the present study, it was found that topical treatment with LBT significantly inhibits psoriasis in mice and maintains skin homeostasis during disease progression by regulating genes associated with keratinocyte proliferation and differentiation, enhancing the PPAR signaling pathway, and upregulating genes and metabolites involved in linoleic acid metabolism. Additionally, LBT suppressed gene expression linked to cytokine activity as well as the Il17, Tnf and MAPK signaling pathways in IMQ‑treated dendritic cells (DCs). These findings underscored LBT's efficacy in reducing IMQ‑induced psoriasis‑like skin inflammation by preserving skin homeostasis and inhibiting inflammatory cytokines in DCs. The present results suggested that topically applied LBT could serve as a promising drug candidate for psoriasis treatment or as an adjunct to biologic therapies to prevent disease relapse.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Research status and future perspectives of IL‑27 in the treatment of stroke (Review). IL - 27在脑卒中治疗中的研究现状及展望（综述）。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-08-01 Epub Date: 2025-05-30 DOI: 10.3892/ijmm.2025.5557

Weiqin Liu, Zhenyou Zou, Wenyang Li, Guang Yang, Jie Zhang, Zhenyu Zhang, Hua Yao

{"title":"Research status and future perspectives of IL‑27 in the treatment of stroke (Review).","authors":"Weiqin Liu, Zhenyou Zou, Wenyang Li, Guang Yang, Jie Zhang, Zhenyu Zhang, Hua Yao","doi":"10.3892/ijmm.2025.5557","DOIUrl":"10.3892/ijmm.2025.5557","url":null,"abstract":"Stroke is a life‑threatening cerebrovascular disorder categorized into two major subtypes: Ischemic and hemorrhagic. Characterized by high morbidity and mortality rates, its clinical management remains challenging due to limited therapeutic options. Interleukin (IL)‑27, a pleiotropic cytokine with demonstrated neuroprotective potential, has emerged as a promising candidate for stroke intervention. IL‑27 exerts immunomodulatory effects within the central nervous system, including suppression of proinflammatory T‑cell proliferation and induction of regulatory T‑cell differentiation. These mechanisms collectively attenuate neuroinflammation, mitigate neuronal apoptosis and prevent neurodegenerative processes. The efficacy of IL‑27 in reducing cerebral damage in both ischemic and hemorrhagic stroke models has been validated, although clinical translation remains to be achieved. The present review summarizes: i) The epidemiology of stroke; ii) the immunoregulatory functions of IL‑27 and its neuroprotective mechanisms across stroke subtypes; iii) innovative brain‑targeted delivery approaches; iv) IL‑27 clinical applicability with supporting evidence; and v) possible risks and solutions in clinical applications. By collating the current knowledge, the present study provides a translational framework for advancing IL‑27‑based therapies in stroke management.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular mechanisms and intervention approaches of heart failure (Review). 心力衰竭的分子机制和干预方法（综述）。

IF 5.7 3区医学

International journal of molecular medicine Pub Date : 2025-08-01 Epub Date: 2025-06-13 DOI: 10.3892/ijmm.2025.5566

Shuang Guo, Yingqing Hu, Li Ling, Zhuangzhuang Yang, Luxuan Wan, Xiaosong Yang, Min Lei, Xiying Guo, Zhanhong Ren

引用次数: 0