Current molecular medicine最新文献

{"title":"LKB1 Mutations Enhance Radiosensitivity in Non-Small Cell Lung Cancer Cells by Inducing G2/M Cell Cycle Phase Arrest.","authors":"Yuanhu Yao, Xiangnan Qiu, Meng Chen, Zhaohui Qin, Xinjun Zhang, Wei Zhang","doi":"10.2174/0115665240280822231221060656","DOIUrl":"10.2174/0115665240280822231221060656","url":null,"abstract":"<p><strong>Background: </strong>Radiosensitivity remains an important factor affecting the clinical outcome of radiotherapy for non-small cell lung cancer (NSCLC). Liver kinase B1 (LKB1) as a tumor suppressor, is one of the most commonly mutated genes in NSCLC. However, the role of LKB1 on radiosensitivity and the possible mechanism have not been elucidated in the NSCLC. In this study, we investigated the regulatory function of LKB1 in the radiosensitivity of NSCLC cells and its possible signaling pathways.</p><p><strong>Methods: </strong>After regulating the expression of LKB1, cell proliferation was determined by Cell Counting Kit-8 (CCK-8) assay. The flow cytometry assay was used to analyse cell cycle distribution. Survival fraction and sensitization enhancement ratio (SER) were generated by clonogenic survival assay. Western blot analysis was used to assess expression levels of LKB1, p53, p21, γ-H2AX and p-Chk2.</p><p><strong>Results: </strong>Our study found that when the NSCLC cells were exposed to ionizing radiation, LKB1 could inhibit NSCLC cell proliferation by promoting DNA double strand break and inducing DNA repair. In addition, LKB1 could induce NSCLC cells G1 and G2/M phase arrest through up-regulating expression of p53 and p21 proteins.</p><p><strong>Conclusion: </strong>This current study demonstrates that LKB1 enhances the radiosensitivity of NSCLC cells via inhibiting NSCLC cell proliferation and inducing G2/M phase arrest, and the mechanism of cell cycle arrest associated with signaling pathways of p53 and p21 probably.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"353-360"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139680768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Narrative Review of Signaling Pathway and Treatment Options for Diabetic Nephropathy.","authors":"Semwal Bhupesh, Neha Chauhan, Verma Jyoti, Kumar Ankit, Singh Sonia, Singh Bhupendra","doi":"10.2174/1566524023666230727093911","DOIUrl":"10.2174/1566524023666230727093911","url":null,"abstract":"<p><strong>Background: </strong>Diabetic nephropathy is a progressive kidney disease that frequently results in end-stage renal disorders and is characterized by proteinuria, albuminuria, decreased filtration, and renal fibrosis. Despite the fact that there are a number of therapeutic alternatives available, DN continues to be the main contributor to end-stage renal disease. Therefore, significant innovation is required to enhance outcomes in DN patients.</p><p><strong>Methods: </strong>Information was collected from online search engines like, Google Scholar, Web of Science, PubMed, Scopus, and Sci-Hub databases using keywords like diabetes, nephropathy, kidney disease, autophagy, etc. Results: Natural compounds have anti-inflammatory and antioxidant properties and impact various signaling pathways. They ameliorate kidney damage by decreasing oxidative stress, inflammatory process, and fibrosis and enhance the antioxidant system, most likely by activating and deactivating several signaling pathways. This review focuses on the role of metabolic memory and various signaling pathways involved in the pathogenesis of DN and therapeutic approaches available for the management of DN. Special attention is given to the various pathways modulated by the phytoconstituents.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"113-131"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9931121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone Deacetylase 2 Stabilizes SPARC-related Modular Calcium Binding 2 to Promote Metastasis and Stemness in Gallbladder Cancer.","authors":"Ji Feng, Xueyong Zheng","doi":"10.2174/0115665240257970231013094101","DOIUrl":"10.2174/0115665240257970231013094101","url":null,"abstract":"<p><strong>Background: </strong>We aimed to investigate the relationship between histone deacetylase 2 (HDAC2) and SPARC-related modular calcium binding 2 (SMOC2) and the role of SMOC2 in gallbladder cancer (GBC).</p><p><strong>Methods: </strong>The expression of HDAC2 and SMOC2 in GBC and normal cells was detected by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), which was also used to detect the mRNA stability of SMOC2. The combination between HDAC2 and SMOC2 was detected by Chromatin immunoprecipitation (ChIP) assay. After silencing and/or overexpressing HDAC2 and SMOC2, cell viability, migration, invasion, and stemness were respectively tested by the Cell Counting Kit-8 (CCK-8), cell scratch, transwell, and sphere-formation assay.</p><p><strong>Results: </strong>In GBC cells, HDAC2 and SMOC2 were highly expressed. HDAC2 combined with SMOC2 promoted mRNA stability of SMOC2. HDAC2 or SMOC2 overexpression promoted GBC cell metastasis and stemness. SMOC2 overexpression rescued the negative effects of silencing HDAC2 in GBC.</p><p><strong>Conclusion: </strong>HDAC2 stabilizes SMOC2 to promote metastasis and stemness in gallbladder cancer.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"56-68"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Potential Therapeutic Applications of CRISPR/Cas9 in the Treatment of Gastrointestinal Cancers.","authors":"Shima Mehrabadi, Faezeh Salmani Izadi, Shiva Pasha, Roozbeh Pourali, Majid Khazaei, Seyed Mahdi Hassanian, Gordon A Ferns, Amir Avan","doi":"10.2174/0115665240243076231116080113","DOIUrl":"10.2174/0115665240243076231116080113","url":null,"abstract":"<p><p>Gastrointestinal (GI) cancer is one the most prevalent types of cancer. Despite current chemotherapy's success, patients with GI cancer continue to have a dismal outcome. The onset and progression of cancer are caused by alterations and the abnormal expression of several families of genes, like tumor-suppressor genes, oncogenes, and chemotherapy-resistant genes. The final purpose of tumor therapy is to inhibit cellular development by modifying mutations and editing the irregular expression of genes It has been reported that CDH1, TP53, KRAS, ARID1A, PTEN, and HLA-B are the commonly mutated genes in GI cancer. Gene editing has become one potential approach for cases with advanced or recurrent CRC, who are nonresponsive to conventional treatments and a variety of driver mutations along with progression cause GI progression. CRISPR/Cas9 technique is a reliable tool to edit the genome and understand the functions of mutations driving GI cancer development. CRISPR/Cas9 can be applied to genome therapy for GI cancers, particularly with reference to molecular-targeted medicines and suppressors. Moreover, it can be used as a therapeutic approach by knocking in/out multiple genes. The use of CRISPR/ Cas9 gene editing method for GI cancer therapy has therefore resulted in some improvements. There are several research works on the role of CRISPR/Cas9 in cancer treatment that are summarized in the following separate sections. Here, the use of CRISPR/Cas9-based genome editing in GI and the use of CRISPR/Cas9 is discussed in terms of Targeting Chemotherapy Resistance-related Genes like; KRAS, TP53, PTEN, and ARID1A.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"278-288"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139511513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nrf2 Inhibits GAPDH/Siah1 Axis to Reduce Inflammatory Reactions and Proliferation of Microglia After Simulating Spinal Cord Injury.","authors":"Chunhe Sha, Feng Pan, Zhiqing Wang, Guohui Liu, Hua Wang, Tianwei Huang, Kai Huang","doi":"10.2174/0115665240280178231218093609","DOIUrl":"10.2174/0115665240280178231218093609","url":null,"abstract":"<p><strong>Objective: </strong>To explore the effect of nuclear factor erythroid 2-related factor 2 (Nrf 2) on microglial inflammatory response and proliferation after spinal cord injury (SCI) through the glyceraldehyde phosphate dehydrogenase (GAPDH) / Seven in absentia homolog 1 (Siah 1) signaling pathway.</p><p><strong>Methods: </strong>Human microglia HMC3 was induced by lipopolysaccharide (LPS) to establish a SCI cell model. Microglia morphology after LPS stimulation was observed by transmission electron microscope (TEM), and cellular Nrf2, GAPDH/Siah1 pathway expression and cell viability were determined. Subsequently, the Nrf2 overexpression plasmid was transfected into microglia to observe changes in cell viability and GAPDH/Siah1 pathway expression.</p><p><strong>Results: </strong>Microglia, mostly amoeba-like, were found to have enlarged cell bodies after LPS stimulation, with an increased number of cell branches, highly expressed Nrf2, GAPDH and Siah1, and decreased cell viability (P<0.05). Up-regulating Nrf2 inhibited the GAPDH/Siah1 axis, decreased inflammatory responses, and enhanced activity in post-SCI microglia (P<0.05).</p><p><strong>Conclusion: </strong>Up-regulating Nrf2 expression can reverse the inflammatory reaction of microglia after LPS stimulation and enhance their activity by inhibiting the GAPDH/ Siah1 axis.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"496-505"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139424502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Explore on the Mechanism of miRNA-146a/TAB1 in the Regulation of Cellular Apoptosis and Inflammation in Ulcerative Colitis Based on NF-κB Pathway.","authors":"Xiaoying Xia, Qian Yang, Xue Han, Yulin Du, Shujun Guo, Mengqing Hua, Fang Fang, Zhigang Ma, Hua Ma, Hui Yuan, Wenjing Tian, Zebang Ding, Yanan Duan, Qi Huo, Yao Li","doi":"10.2174/0115665240273807231122052445","DOIUrl":"10.2174/0115665240273807231122052445","url":null,"abstract":"<p><strong>Objective: </strong>Ulcerative colitis (UC) is a chronic non-specific inflammatory disease of the rectum and colon with unknown etiology. A growing number of evidence suggest that the pathogenesis of UC is related to excessive apoptosis and production of inflammatory cytokines. However, the functions and molecular mechanisms associated with UC remain unclear.</p><p><strong>Materials and methods: </strong>The <i>in vivo</i> and <i>in vitro</i> models of UC were established in this study. MiRNA or gene expression was measured by qRT-PCR assay. ELISA, CCK-8, TUNEL, and flow cytometry assays were applied for analyzing cellular functions. The interactions between miR-146a and TAB1 were verified by luciferase reporter and miRNA pull-down assays.</p><p><strong>Results: </strong>MiR-146a was obviously increased in UC patients, DSS-induced colitis mice, and TNF-α-induced YAMC cells, when compared to the corresponding controls. MiR- 146a knockdown inhibited the inflammatory response and apoptosis in DSS-induced colitis mice and TNF-α-induced YAMC cells. Mechanistically, we found that TAB1 was the target of miR-146a and miR-146a knockdown suppressed the activation of NF-κB pathway in UC. More importantly, TAB1 could overturn the inhibitory effect of antagomiR-146a on cell apoptosis and inflammation in UC.</p><p><strong>Conclusion: </strong>MiR-146a knockdown inhibited cell apoptosis and inflammation via targeting TAB1 and suppressing NF-κB pathway, suggesting that miR-146a may be a new therapeutic target for UC treatment.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"330-342"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implication of Thioredoxin 1 and Glutaredoxin 1 in H₂O₂-induced Phosphorylation of JNK and p38 MAP Kinases.","authors":"Efthymios Poulios, Vasiliki Roupaka, Constantinos Giaginis, Dimitrios Galaris, Giannis Spyrou","doi":"10.2174/0115665240271103231127072635","DOIUrl":"10.2174/0115665240271103231127072635","url":null,"abstract":"<p><strong>Background: </strong>Aerobic organisms continuously generate small amounts of Reactive Oxygen Species (ROS), which are involved in the oxidation of sensitive cysteine residues in proteins, leading to the formation of disulfide bonds. Thioredoxin (Trx1) and Glutaredoxin (Grx1) represent key antioxidant enzymes reducing disulfide bonds.</p><p><strong>Objective: </strong>In this work, we have focused on the possible protective effect of Trx1 and Grx1 against oxidative stress-induced DNA damage and apoptosis-signaling, by studying the phosphorylation of MAP kinases.</p><p><strong>Methods: </strong>Trx1 and Grx1 were overexpressed or silenced in cultured H1299 non-small cell lung cancer epithelial cells. We examined cell growth, DNA damage, and the phosphorylation status of MAP kinases following treatment with H₂O₂.</p><p><strong>Results: </strong>Overexpression of both Trx1 and Grx1 had a significant impact on the growth of H1299 cells and provided protection against H₂O₂-induced toxicity, as well as acute DNA single-strand breaks. Conversely, silencing of these proteins exacerbated DNA damage. Furthermore, overexpression of Trx1 and Grx1 inhibited the rapid phosphorylation of JNK (especially at 360 min of treatment, ****p=0.004 and **p=0.0033 respectively) and p38 MAP kinases (especially at 360 min of treatment, ****p<0.0001 and ***p=0.0008 respectively) during H₂O₂ exposure, while their silencing had the opposite effect (especially at 360 min of treatment, ****p<0.0001).</p><p><strong>Conclusion: </strong>These results suggest that both Trx1 and Grx1 have protective roles against H₂O₂ induced toxicity, emphasizing their significance in mitigating oxidative stress-related cellular damage.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"305-319"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139511341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Multiple Roles of Heat Shock Proteins in the Development of Inflammatory Bowel Disease.","authors":"Jinfeng Su, Haiyan Wang, Zun Wang","doi":"10.2174/0115665240286793240306053111","DOIUrl":"10.2174/0115665240286793240306053111","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), a chronic inflammatory condition of the human intestine, comprises Crohn's disease (CD) and ulcerative colitis (UC). IBD causes severe gastrointestinal symptoms and increases the risk of developing colorectal carcinoma. Although the etiology of IBD remains ambiguous, complex interactions between genetic predisposition, microbiota, epithelial barrier, and immune factors have been implicated. The disruption of intestinal homeostasis is a cardinal characteristic of IBD. Patients with IBD exhibit intestinal microbiota dysbiosis, impaired epithelial tight junctions, and immune dysregulation; however, the relationship between them is not completely understood. As the largest body surface is exposed to the external environment, the gastrointestinal tract epithelium is continuously subjected to environmental and endogenous stressors that can disrupt cellular homeostasis and survival. Heat shock proteins (HSPs) are endogenous factors that play crucial roles in various physiological processes, such as maintaining intestinal homeostasis and influencing IBD progression. Specifically, HSPs share an intricate association with microbes, intestinal epithelium, and the immune system. In this review, we aim to elucidate the impact of HSPs on IBD development by examining their involvement in the interactions between the intestinal microbiota, epithelial barrier, and immune system. The recent clinical and animal models and cellular research delineating the relationship between HSPs and IBD are summarized. Additionally, new perspectives on IBD treatment approaches have been proposed.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"132-145"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140093581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Systematic Review of the Impact of Resveratrol on Viral Hepatitis and Chronic Viral Hepatitis-related Hepatocellular Carcinoma.","authors":"Mohammad Darvishi, Majid Nouri, Rasoul Rahimi, Saeid Heidari-Soureshjani, Seyed Mahmoud Reza Hashemi Rafsanjani","doi":"10.2174/0115665240284347240125072555","DOIUrl":"10.2174/0115665240284347240125072555","url":null,"abstract":"<p><strong>Background: </strong>Resveratrol (RSV) is used for the treatment of various diseases due to their anti-inflammatory and antioxidant activities. However, its beneficial aspects on viral hepatitis have been less investigated.</p><p><strong>Objective: </strong>This report reviews the impact of resveratrol on viral hepatitis and chronic viral hepatitis-related hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>The systematic review was performed and reported according to the PRISMA 2020 statement. Several core databases, such as Cochrane Library, PubMed, Web of Science, EMBASE, and Scopus, were used for search on September 6, 2023. After extraction of the data, the desired information of the full text of the studies was recorded in Excel, and the outcomes and mechanisms were reviewed.</p><p><strong>Results: </strong>RSV inhibits viral replication through anti-HCV NS3 helicase activity, maintains redox homeostasis via glutathione (GSH) synthesis, improves T and B cell activity, and suppresses miR-155 expression. It also enhances viral replication by enhancing hepatitis C virus (HCV) RNA transcription, activating sirtuin-1 (SIRT1), which can increase peroxisome proliferator-activated receptor (PPAR), and SIRT1 activates the HBV X protein (HBx). Moreover, RSV is responsible for hepatitis-related HCC proliferation via suppression of mammalian target of rapamycin (mTOR), SIRT1 up-regulation, inhibiting expression of HBx, and reducing expression of cyclin D1.</p><p><strong>Conclusion: </strong>Despite the promising properties of RSV in inhibiting hepatitis-related HCC cell proliferation, its antiviral effects in viral hepatitis are controversial. The antihepatitis behaviors of RSV are mainly dose-dependent, and in some studies, activating some hepatoprotective pathways increases the transcription and replication of chronic HBV and HCV. Therefore, healthcare providers should be aware of viral hepatitis before using RSV supplements.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"589-604"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139905282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem Cells as a Novel Source for Regenerative Medicinal Applications in Alzheimer's Disease: An Update.","authors":"Kratika Pandey, Priyanka Srivastava, Swaroop Kumar Pandey, Surabhi Johari, Priyanka Bhatnagar, Madhavi Sonane, Anuja Mishra","doi":"10.2174/0115665240334785240913071442","DOIUrl":"10.2174/0115665240334785240913071442","url":null,"abstract":"<p><p>Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by loss of the neurons, excessive accumulation of misfolded Aβ and Tau proteins, and degeneration of neural synapses, primarily occurring in the neocortex and the hippocampus regions of the brain. AD Progression is marked by cognitive deterioration, memory decline, disorientation, and loss of problem-solving skills, as well as language. Due to limited comprehension of the factors contributing to AD and its severity due to neuronal loss, even today, the medications approved by the U.S. Food and Drug Administration (FDA) are not precisely efficient and curative. Stem cells possess great potential in aiding AD due to their self-renewal, proliferation, and differentiation properties. Stem cell therapy can aid by replacing the lost neurons, enhancing neurogenesis, and providing an enriched environment to the pre-existing neural cells. Stem cell therapy has provided us with promising results in regard to the animal AD models, and even pre-clinical studies have shown rather positive results. Cell replacement therapies are potential curative means to treat AD, and there are a number of undergoing human clinical trials to make Stem Cell therapy accessible for AD patients. In this review, we aim to discuss the AD pathophysiology and varied stem cell types and their application.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":"146-166"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}