Experimental and Molecular Medicine最新文献

SLC27A2 marks lipid peroxidation in nasal epithelial cells driven by type 2 inflammation in chronic rhinosinusitis with nasal polyps. SLC27A2标志着慢性鼻窦炎伴鼻息肉2型炎症驱动的鼻上皮细胞脂质过氧化。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-07 DOI: 10.1038/s12276-025-01440-1

Jaewoo Park, Jung Yeon Jang, Jeong Heon Kim, Se Eun Yi, Yeong Ju Lee, Myeong Sang Yu, Yoo-Sam Chung, Yong Ju Jang, Ji Heui Kim, Kyuho Kang

{"title":"SLC27A2 marks lipid peroxidation in nasal epithelial cells driven by type 2 inflammation in chronic rhinosinusitis with nasal polyps.","authors":"Jaewoo Park, Jung Yeon Jang, Jeong Heon Kim, Se Eun Yi, Yeong Ju Lee, Myeong Sang Yu, Yoo-Sam Chung, Yong Ju Jang, Ji Heui Kim, Kyuho Kang","doi":"10.1038/s12276-025-01440-1","DOIUrl":"https://doi.org/10.1038/s12276-025-01440-1","url":null,"abstract":"Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by persistent inflammation and epithelial cell dysfunction, but the underlying molecular mechanisms remain poorly understood. Here we show that dysregulated lipid metabolism and increased lipid peroxidation in nasal polyp epithelial cells contribute to the pathogenesis of CRSwNP. Integrated analysis of bulk and single-cell RNA sequencing data reveals upregulation of SLC27A2/FATP2 in nasal polyp epithelium, which correlates with increased lipid peroxidation. SLC27A2-positive epithelial cells exhibit enriched expression of lipid peroxidation pathway genes and enhanced responsiveness to IL-4/IL-13 signaling from Th2 and ILC2 cells. Inhibition of IL-4/IL-13 signaling by dupilumab reduces expression of lipid peroxidation-associated genes, including SLC27A2. In eosinophilic CRSwNP, SLC27A2 expression correlates with disease severity. Pharmacological inhibition of FATP2 in air-liquid interface cultures of nasal epithelial cells decreases expression of IL13RA1 and lipid peroxidation-related genes. Our findings identify FATP2-mediated lipid peroxidation as a key driver of epithelial dysfunction and inflammation in CRSwNP, providing new insights into disease mechanisms and potential therapeutic targets.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Hepatocyte TM4SF5-mediated cytosolic NCOA3 stabilization and macropinocytosis support albumin uptake and bioenergetics for hepatocellular carcinoma progression. 肝细胞tm4sf5介导的胞质NCOA3稳定和巨噬细胞作用支持白蛋白摄取和肝细胞癌进展的生物能量学。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-04 DOI: 10.1038/s12276-025-01438-9

Haesong Lee, Ji Eon Kim, Eun-Ae Shin, Yangie Pinanga, Kyung-Hee Pyo, Eun Hae Lee, Wonsik Kim, Soyeon Kim, Chang Sup Lim, Kyung Chul Yoon, Jung Weon Lee

{"title":"Hepatocyte TM4SF5-mediated cytosolic NCOA3 stabilization and macropinocytosis support albumin uptake and bioenergetics for hepatocellular carcinoma progression.","authors":"Haesong Lee, Ji Eon Kim, Eun-Ae Shin, Yangie Pinanga, Kyung-Hee Pyo, Eun Hae Lee, Wonsik Kim, Soyeon Kim, Chang Sup Lim, Kyung Chul Yoon, Jung Weon Lee","doi":"10.1038/s12276-025-01438-9","DOIUrl":"10.1038/s12276-025-01438-9","url":null,"abstract":"Transmembrane 4 L six family member 5 (TM4SF5) is involved in hepatocellular carcinoma (HCC) development and progression. Although TM4SF5 also promotes migration and invasion, it remains unclear how the metabolic context affects metastatic potential. Here we explored how TM4SF5 affects albumin uptake for HCC progression using TM4SF5 knockout or reintroduced hepatocyte and animal systems. Serum-deprived hepatocytes formed filopodia-like processes depending on TM4SF5 expression, which was altered by albumin replenishment for membranous PIP3-dependent macropinocytosis. Macropinocytosis required nuclear receptor coactivator 3 (NCOA3) stabilized in the cytosol and PTEN inactivation via binding to TM4SF5WT. TM4SF5-mediated albumin uptake led to ATP-linked respiration and cellular migration. Tumor tissues from liver-orthotopically xenografted mice fed a high protein diet or human liver cancer tissues showed TM4SF5-dependent macropinocytosis and NCOA3-correlated metastatic features, unlike mice fed a normal chow diet or human nontumor regions. These observations indicate that serum albumin availability to TM4SF5-positive HCC could support multifocality and intrahepatic metastasis, which may provide insights into clinical observations of multiple small tumor nodules surrounded by areas with high serum albumin levels.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Redefining the immune landscape of hepatitis A virus infection. 重新定义甲型肝炎病毒感染的免疫景观。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-02 DOI: 10.1038/s12276-025-01431-2

Ombretta Colasanti, Hosun Yu, Volker Lohmann, Eui-Cheol Shin

引用次数: 0

Lactobacillus paracasei-derived extracellular vesicles reverse molecular and behavioral deficits in mouse models of autism spectrum disorder. 副干酪乳杆菌衍生的细胞外囊泡逆转自闭症谱系障碍小鼠模型的分子和行为缺陷。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01429-w

Jin-Young Park, Eun-Hwa Lee, Ji-Eun Kim, Jae-Won Paeng, Jin-Chul Paeng, Tae-Kyung Kim, Yoon-Keun Kim, Pyung-Lim Han

{"title":"Lactobacillus paracasei-derived extracellular vesicles reverse molecular and behavioral deficits in mouse models of autism spectrum disorder.","authors":"Jin-Young Park, Eun-Hwa Lee, Ji-Eun Kim, Jae-Won Paeng, Jin-Chul Paeng, Tae-Kyung Kim, Yoon-Keun Kim, Pyung-Lim Han","doi":"10.1038/s12276-025-01429-w","DOIUrl":"https://doi.org/10.1038/s12276-025-01429-w","url":null,"abstract":"Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders characterized by social communication deficits and repetitive behaviors. Although our current understanding the mechanisms underlying ASD is growing, effective treatment options are still underdevelopment. Extracellular vesicles derived from the probiotic Lactobacillus paracasei (LpEV) have shown neuroprotective effects in both in vitro and in vivo models. Here we investigate whether LpEV can alleviate core symptoms in genetic ASD models that exhibit accumulated developmental deficits. Dopamine receptor D2 (Drd2)-knockout (KO) mice exhibit social behavior deficits and excessive grooming, core symptoms of ASD. LpEV treatment significantly improves these autistic-like behaviors in Drd2-KO mice, suggesting that LpEVs can mitigate the persistent dysregulation of signaling pathways in these mice. RNA sequencing followed by Gene Ontology enrichment analysis of LpEV-treated Drd2-KO mice identifies distinct groups of genes altered in the brain of Drd2-KO mice, which were reversed by LpEV treatment. Notably, a high proportion of these genes overlap significantly with known ASD genes in the SFARI database, strengthening the potential of LpEV to target relevant pathways in ASD. Further investigation identifies oxytocin and oxytocin receptor (Oxtr) as potential therapeutic targets. LpEV treatment significantly improves autistic-like behaviors in Oxtr-KO heterozygous mice, adenylyl cyclase-5 KO mice and Shank3-KO mice, suggesting its therapeutic potential to target ASD through broader mechanisms beyond a single gene pathway. These results highlight the therapeutic potential of LpEV in reversing the accumulated dysregulated signaling pathways leading to ASD symptoms and improving autistic-like behaviors.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

PGC-1α mediates migrasome secretion accelerating macrophage-myofibroblast transition and contributing to sepsis-associated pulmonary fibrosis. PGC-1α介导迁移小体分泌，加速巨噬细胞-肌成纤维细胞转化，促进败血症相关肺纤维化。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01426-z

Yawen Peng, Shuya Mei, Xiaohui Qi, Ri Tang, Wenyu Yang, Jinhua Feng, Yang Zhou, Xi Huang, Guojun Qian, Shunpeng Xing, Yuan Gao, Qiaoyi Xu, Zhengyu He

{"title":"PGC-1α mediates migrasome secretion accelerating macrophage-myofibroblast transition and contributing to sepsis-associated pulmonary fibrosis.","authors":"Yawen Peng, Shuya Mei, Xiaohui Qi, Ri Tang, Wenyu Yang, Jinhua Feng, Yang Zhou, Xi Huang, Guojun Qian, Shunpeng Xing, Yuan Gao, Qiaoyi Xu, Zhengyu He","doi":"10.1038/s12276-025-01426-z","DOIUrl":"https://doi.org/10.1038/s12276-025-01426-z","url":null,"abstract":"Sepsis-associated pulmonary fibrosis (SAPF) is a critical pathological stage in the progression of sepsis-induced acute respiratory distress syndrome. While the aggregation and activation of lung fibroblasts are central to the initiation of pulmonary fibrosis, the macrophage-myofibroblast transition (MMT) has recently been identified as a novel source of fibroblasts in this context. However, the mechanisms driving MMT remain inadequately understood. Given the emerging role of migrasomes (novel extracellular vesicles mediating intercellular communication), we investigated their involvement in pulmonary fibrosis. Here we utilized a lipopolysaccharide-induced SAPF mouse model and an in vitro co-culture system of fibroblasts and macrophages to observe the MMT process during SAPF. We found that lipopolysaccharide exposure suppresses PGC-1α expression in lung fibroblasts, resulting in mitochondrial dysfunction and the accumulation of cytosolic mitochondrial DNA (mtDNA). This dysfunction promotes the secretion of mtDNA-containing migrasomes, which, in turn, initiate the MMT process and contribute to fibrosis progression. Notably, the activation of PGC-1α mitigates mitochondrial dysfunction, reduces mtDNA-migrasome release, inhibits MMT and alleviates SAPF. In conclusion, our study identifies the suppression of PGC-1α in lung fibroblasts and the subsequent release of mtDNA migrasomes as a novel mechanism driving MMT in SAPF. These findings suggest that targeting the crosstalk between fibroblasts and immune cells mediated by migrasomes could represent a promising therapeutic strategy for SAPF.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Conversation between skin microbiota and the host: from early life to adulthood. 皮肤微生物群与宿主之间的对话：从生命早期到成年。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01427-y

Jimin Cha, Tae-Gyun Kim, Ji-Hwan Ryu

引用次数: 0

MSK1 promotes colorectal cancer metastasis by increasing Snail protein stability through USP5-mediated Snail deubiquitination. MSK1通过usp5介导的蜗牛去泛素化，提高蜗牛蛋白的稳定性，从而促进结直肠癌转移。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01433-0

Keun-Seok Hong, Ki-Jun Ryu, Hyemin Kim, Minju Kim, Seung-Ho Park, Taeyoung Kim, Jung Wook Yang, Cheol Hwangbo, Kwang Dong Kim, Young-Jun Park, Jiyun Yoo

{"title":"MSK1 promotes colorectal cancer metastasis by increasing Snail protein stability through USP5-mediated Snail deubiquitination.","authors":"Keun-Seok Hong, Ki-Jun Ryu, Hyemin Kim, Minju Kim, Seung-Ho Park, Taeyoung Kim, Jung Wook Yang, Cheol Hwangbo, Kwang Dong Kim, Young-Jun Park, Jiyun Yoo","doi":"10.1038/s12276-025-01433-0","DOIUrl":"https://doi.org/10.1038/s12276-025-01433-0","url":null,"abstract":"Mitogen- and stress-activated protein kinase 1 (MSK1), a Ser/Thr kinase, phosphorylates nuclear proteins to increase their stability and DNA-binding affinity. Despite the role of MSK1 in promoting cancer progression in colorectal cancer (CRC), the precise molecular mechanisms remain unelucidated. Here we show that MSK1 expression induces the epithelial-mesenchymal transition (EMT) process and increases CRC cell metastasis. Furthermore, we discovered that MSK1 interacts with Snail, a key EMT regulator, and increases its stability by inhibiting ubiquitin-mediated proteasomal degradation. Importantly, MSK1 increased Snail protein stability by promoting deubiquitination rather than inhibiting its ubiquitination. Finally, we identified USP5 as an essential deubiquitinase that binds to Snail protein phosphorylated by MSK1. Based on the experimental data, in CRC, MSK1-Snail-USP5 axis can promote EMT and metastasis of CRC. Together, our findings provide potential biomarkers and novel therapeutic targets for further research in CRC.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Systematic genetic assessment of hearing loss using whole-genome sequencing identifies pathogenic variants. 使用全基因组测序对听力损失进行系统遗传评估，确定致病变异。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01428-x

Jung Ah Kim, Seung Hyun Jang, Sun Yung Joo, Se Jin Kim, Jae Young Choi, Jinsei Jung, Heon Yung Gee

{"title":"Systematic genetic assessment of hearing loss using whole-genome sequencing identifies pathogenic variants.","authors":"Jung Ah Kim, Seung Hyun Jang, Sun Yung Joo, Se Jin Kim, Jae Young Choi, Jinsei Jung, Heon Yung Gee","doi":"10.1038/s12276-025-01428-x","DOIUrl":"10.1038/s12276-025-01428-x","url":null,"abstract":"Hearing loss is a clinically and genetically heterogeneous sensorineural disease that affects approximately 1 out of 1000 newborns. For the molecular diagnosis of genetic hearing loss, target panel or whole-exome sequencing (WES) have been widely used due to their cost-effectiveness and efficacy. Despite the advantages of WES, the plausible diagnoses in a substantial number of patients remain elusive due to its limited coverage. Here we utilized whole-genome sequencing (WGS) on a large cohort of individuals with hearing loss to overcome the drawbacks of WES and find the advantages of WGS. We implemented a systematic workflow to identify coding region variants, cryptic splice variants, mitochondrial variants, copy number variants, cis-regulatory variants and transposable element insertions. WGS was conducted on 140 families with hearing loss. Causative variations were identified in 37 of these families, accounting for 26% of the total. WGS possessed the capability to find genetic variations that are not identifiable using WES. The identified variants by WGS in this study encompassed aberrant splicing variants in EYA1 and CDH23, mitochondrial variants in MT-RNR1 and MT-CO1, structural variants in STRC, and Alu insertion in SLC17A8. These findings highlight the benefits of WGS. With the decreasing cost of WGS, its usage will become more prevalent, allowing more precise identification of the genetic causes of hearing loss.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Human neuron chimeric mice reveal impairment of DVL-1-mediated neuronal migration by sevoflurane and potential treatment by rTMS. 七氟醚对人神经元嵌合小鼠dvl -1介导的神经元迁移的损伤及rTMS的潜在治疗作用。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01425-0

Youyi Zhao, Ya Zhao, Lirong Liang, Andi Chen, Yuqian Li, Ke Liu, Rougang Xie, Honghui Mao, Boyang Ren, Bosong Huang, Changhong Shi, Zhicheng Shao, Shengxi Wu, Yazhou Wang, Hui Zhang

{"title":"Human neuron chimeric mice reveal impairment of DVL-1-mediated neuronal migration by sevoflurane and potential treatment by rTMS.","authors":"Youyi Zhao, Ya Zhao, Lirong Liang, Andi Chen, Yuqian Li, Ke Liu, Rougang Xie, Honghui Mao, Boyang Ren, Bosong Huang, Changhong Shi, Zhicheng Shao, Shengxi Wu, Yazhou Wang, Hui Zhang","doi":"10.1038/s12276-025-01425-0","DOIUrl":"https://doi.org/10.1038/s12276-025-01425-0","url":null,"abstract":"Whether early exposure to general anesthetics hurts human brain development is still under discussion. Animal studies have documented multiple neurotoxicities of repeated/prolonged exposure to sevoflurane (Sev, a commonly used pediatric anesthetic) at the neonatal stage. Its effects on human neural development remain elusive. Here, by investigating neural progenitor cells derived from two human embryonic stem cell lines, human cerebral organoids and human neuronal chimeric mice, we found that, although Sev inhibits neuronal differentiation and synaptogenesis of human neural progenitor cells in vitro, it only inhibits human neuronal migration in vivo. Chemogenetic activation of human neurons rescued the defects of cell migration and social dysfunction of Sev-pretreated human neuronal chimeric mice. Mechanistically, Sev inhibits DVL-1/Ca2+ signaling and multiple cell migration-related genes. Overexpressing DVL-1 enhanced the Ca2+ response, neuronal migration and social function of Sev-pretreated chimeric mice. Furthermore, specific modulation of human neurons by high-frequency transcranial magnetic stimulation not only activated DVL-1/Ca2+ signaling but also improved human neuronal migration and social function in chimeric mice. Our data demonstrate that early Sev exposure is toxic to human neuronal migration via inhibiting DVL-1 signaling and that transcranial magnetic stimulation could be potentially therapeutic.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Pim1 promotes the maintenance of bone homeostasis by regulating osteoclast function. Pim1通过调节破骨细胞功能促进骨稳态的维持。

IF 9.5 2区医学

Experimental and Molecular Medicine Pub Date : 2025-04-01 DOI: 10.1038/s12276-025-01421-4

Jeongin Seo, Ryeojin Ko, Minhee Kim, Jeongmin Seo, Hana Lee, Doyong Kim, Woojin Jeong, Han Sung Kim, Soo Young Lee

{"title":"Pim1 promotes the maintenance of bone homeostasis by regulating osteoclast function.","authors":"Jeongin Seo, Ryeojin Ko, Minhee Kim, Jeongmin Seo, Hana Lee, Doyong Kim, Woojin Jeong, Han Sung Kim, Soo Young Lee","doi":"10.1038/s12276-025-01421-4","DOIUrl":"https://doi.org/10.1038/s12276-025-01421-4","url":null,"abstract":"The Pim1 (proviral integration site for Moloney leukemia virus 1) protein is a serine/threonine kinase that is essential for cell proliferation, apoptosis and innate immune responses. Here we show that Pim1 promotes osteoclast resorptive function without affecting osteoclast numbers. Specifically, we found that mice lacking Pim1 (Pim1-/-) developed increased trabecular bone mass and indices such as trabecular bone-mass density. This was due to the direct phosphorylation of TRAF6 by Pim1 in mature osteoclasts, which activated the Akt-GSK3β signaling pathway. This, in turn, promoted the acetylation and consequent stabilization of microtubules, which permitted the formation of the osteoclast sealing zone. In vivo experiments then showed that, when mice with lipopolysaccharide-induced bone loss or tumor-induced osteolysis were treated with SGI-1776, a Pim1 inhibitor that is more selective for Pim1, the bone loss was significantly ameliorated. Thus, Pim1 plays an important role in osteoclast function and may be a therapeutic target for bone-related diseases.","PeriodicalId":50466,"journal":{"name":"Experimental and Molecular Medicine","volume":" ","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143754918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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