IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.194068

Kexin Lei, Qi Yin, Qiwen Li, Qian Wang, Zhong Zhang, Fei Xue, Ruoshi Xu, Xinyi Zhou, Lin Peng, Shoichiro Kokabu, Shuibin Lin, Quan Yuan

引用次数: 0

DNM2 lipid binding drives centronuclear myopathy and represents a potential therapeutic target. DNM2脂质结合驱动核中心性肌病，并代表一个潜在的治疗靶点。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.204423

Raquel Gómez-Oca, Xènia Massana-Muñoz, David Reiss, Juliana De Carvalho Neves, Nadege Diedhiou, Roberto Silva-Rojas, Belinda S Cowling, Marie Goret, Jocelyn Laporte

{"title":"DNM2 lipid binding drives centronuclear myopathy and represents a potential therapeutic target.","authors":"Raquel Gómez-Oca, Xènia Massana-Muñoz, David Reiss, Juliana De Carvalho Neves, Nadege Diedhiou, Roberto Silva-Rojas, Belinda S Cowling, Marie Goret, Jocelyn Laporte","doi":"10.1172/jci.insight.204423","DOIUrl":"https://doi.org/10.1172/jci.insight.204423","url":null,"abstract":"Centronuclear myopathies (CNMs) are rare congenital disorders characterized by muscle weakness, fiber hypotrophy, and organelle mislocalization. Most cases arise from mutations in MTM1 or DNM2, encoding myotubularin and dynamin-2, respectively. DNM2 is a GTPase that binds lipids, oligomerizes around membranes, and mediates fission. We previously showed that DNM2 levels are elevated in MTM1-CNM patients and Mtm1-/y mice, and that normalizing DNM2 rescues disease phenotypes. However, the specific DNM2 functions driving pathology remain unclear. Here, we expressed AAV-delivered WT and DNM2 mutants in WT and Mtm1-/y mouse muscles to disrupt specific DNM2 molecular functions. In WT mice, overexpression of WT DNM2 and most mutants induced CNM-like phenotypes, including reduced force, fiber hypotrophy, and centralized nuclei, consistent with gain-of-function mechanisms. The lipid-binding-defective mutant K562E did not induce disease-like phenotype. In Mtm1-/y mice, K562E mutant markedly improved muscle force, mass, and fiber size, while others failed to rescue. Therefore, we generated Mtm1-/y Dnm2K562E/+ mice, which showed full rescue of survival, motor function, and muscle force, with improved muscle mass, fiber size, and organelle positioning despite persistently elevated DNM2 levels. This study reveals that DNM2 lipid binding, not protein abundance or GTPase activity, drives pathology, and represents the most rational therapeutic target for DNM2 therapy in MTM1-CNM.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Pulsatile flow dynamics maintain pulmonary artery architecture. 脉搏血流动力学维持肺动脉结构。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.201797

Stephen B Spurgin, Lauren Thai, Tina C Wan, Christopher P Chaney, Mitzy A Cowdin, Surendranath Veeram Reddy, Tarique Hussain, Munes Fares, M Luisa Iruela-Arispe, Thomas Carroll, Andrew D Spearman, Ondine Cleaver

{"title":"Pulsatile flow dynamics maintain pulmonary artery architecture.","authors":"Stephen B Spurgin, Lauren Thai, Tina C Wan, Christopher P Chaney, Mitzy A Cowdin, Surendranath Veeram Reddy, Tarique Hussain, Munes Fares, M Luisa Iruela-Arispe, Thomas Carroll, Andrew D Spearman, Ondine Cleaver","doi":"10.1172/jci.insight.201797","DOIUrl":"https://doi.org/10.1172/jci.insight.201797","url":null,"abstract":"Single-ventricle congenital heart disease (SV-CHD) is a uniformly lethal condition requiring the Glenn surgery, which as a side effect eliminates arterial pulsatility and contributes to pulmonary vascular complications. In Glenn patients, we quantified pulsatility loss in each dimension of force (flow, pressure, and stretch) using cardiac catheterization and MRI. To model and investigate the individual impact of each dimension of pulsatility loss on the pulmonary vasculature, we applied isolated pulsatile and non-pulsatile mechanical stimuli to pulmonary artery endothelial cells (ECs) in vitro. We found that each dimension of force triggered distinct transcriptional responses, revealing force-specific regulation of structural and signaling pathways. Pulsatile stretch uniquely stimulated EC secretion of PDGFB, a key driver of vascular smooth muscle cell (vSMC) recruitment. In a rat Glenn model, loss of pulsatility led to vascular wall thinning, loss of EC PDGFB, and reduced activation of smooth muscle PDGFBRβ, confirming in vivo relevance. Our findings uncover a mechanistic link between endothelial stretch sensing and PDGFB-mediated EC-vSMC crosstalk, essential for maintaining pulmonary artery architecture. Clinically, these insights suggest that restoring or mimicking pulsatile forces may help preserve vascular integrity and prevent remodeling in patients with SV-CHD.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Base editing and nanoparticle transfection of airway cell types essential for treatment of cystic fibrosis. 碱基编辑和纳米颗粒转染对治疗囊性纤维化必不可少的气道细胞类型。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.198563

Erin W Kavanagh, Anya T Joynt, Audrey R Pion, Alice C Eastman, Alianna I Parr, Katherine L Starego, Manav Jain, Sydney R Shannon, Edwin J Yoo, Gregory A Newby, Stephany Y Tzeng, Neeraj Sharma, Jordan J Green, Garry R Cutting

{"title":"Base editing and nanoparticle transfection of airway cell types essential for treatment of cystic fibrosis.","authors":"Erin W Kavanagh, Anya T Joynt, Audrey R Pion, Alice C Eastman, Alianna I Parr, Katherine L Starego, Manav Jain, Sydney R Shannon, Edwin J Yoo, Gregory A Newby, Stephany Y Tzeng, Neeraj Sharma, Jordan J Green, Garry R Cutting","doi":"10.1172/jci.insight.198563","DOIUrl":"https://doi.org/10.1172/jci.insight.198563","url":null,"abstract":"Cystic fibrosis (CF) is a life-limiting genetic disorder caused by deleterious variants in the CFTR gene that results in altered mucus impairing the airway epithelia. Durable correction of these variants in airway cells remains a therapeutic challenge for about 10% of individuals unresponsive to CFTR modulators. A common disease-causing CFTR splice site variant, 3120+1G>A, was corrected in primary CF airway cells using base editor RNAs. Single-cell RNA sequencing revealed a remarkable increase in detectable CFTR transcript in most CF airway epithelial cell types resulting in notable enrichment of CFTR-expressing ionocytes and secretory goblet cells. Progenitor basal cell subtypes were edited, but they decreased as a fraction of total cells and CFTR-expressing cells compared with unedited cells. CRISPR base editors delivered by polymeric nanoparticles (PNPs) facilitated functional rescue of CFTR to clinically meaningful levels in immortalized and primary airway cells. PNPs delivered GFP-encoding RNA to progenitor airway cells in fully differentiated airway cultures. Vitronectin was a major component of the PNP corona that formed in vivo, but preincubation with vitronectin did not enhance delivery. Together, these findings validate a scalable, nonviral platform with compelling translational promise for treating CF and other respiratory diseases involving respiratory epithelial cell dysfunction.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ATP7A-fibulin-4 complex delivers copper in the Golgi to activate LOX in renal fibrosis. atp7a -纤维蛋白-4复合物在高尔基体中传递铜以激活肾纤维化中的LOX。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.199028

Wenqian Zhou, Yan Zheng, Yuqing Liu, Jing Liu, Yiguo Liu, Yangyang Niu, Ying Yu, Xiaoqin Zhang, Yingying Zhang, Chen Yu

{"title":"ATP7A-fibulin-4 complex delivers copper in the Golgi to activate LOX in renal fibrosis.","authors":"Wenqian Zhou, Yan Zheng, Yuqing Liu, Jing Liu, Yiguo Liu, Yangyang Niu, Ying Yu, Xiaoqin Zhang, Yingying Zhang, Chen Yu","doi":"10.1172/jci.insight.199028","DOIUrl":"https://doi.org/10.1172/jci.insight.199028","url":null,"abstract":"Lysyl oxidase (LOX) is a copper-dependent monoamine oxidase whose primary function is the covalent cross-linking of collagen and elastin in the extracellular matrix (ECM). However, the regulation of LOX activity in renal fibrosis is not well understood. Here, our study showed that (a) LOX expression and ECM cross-linking were markedly increased in fibrotic kidneys. Reduction of copper levels in the Golgi apparatus by treatment with the copper chelator tetrathiomolybdate or by specific knockdown of copper transporter 1 (CTR1) decreased LOX activity and ameliorated renal fibrosis. (b) Overexpression of ATP7A caused an elevation of copper ions within the Golgi apparatus, resulting in increased LOX activity and enhanced ECM crosslinking, thereby promoting the progression of renal fibrosis. Knockdown of ATP7A showed the opposite result. (c) FBLN4 was essential for the ATP7A-mediated transfer of copper to LOX and formed a ternary complex of ATP7A-FBLN4-LOX. Our research revealed that high ATP7A expression induced copper overload in the Golgi apparatuses. FBLN4 then assisted ATP7A in transporting this excess copper to LOX, resulting in LOX overactivation. This, in turn, catalyzed the cross-linking of ECM components, thereby accelerating renal fibrosis.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Progressive HNF1A-MODY pathophysiology revealed by a translational mouse model. 翻译小鼠模型揭示的进行性HNF1A-MODY病理生理。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.198095

Isaline Louvet, Ana Acosta-Montalvo, Chiara Saponaro, Maria Moreno-Lopez, Sana Douffi, Abdelkrim El Karchaoui, Gianni Pasquetti, Julien Thevenet, Nathalie Delalleau, Valery Gmyr, Paolo Giacobini, Stéphanie Espiard, Julie Kerr-Conte, François Pattou, Adrian Liston, Caroline Bonner

{"title":"Progressive HNF1A-MODY pathophysiology revealed by a translational mouse model.","authors":"Isaline Louvet, Ana Acosta-Montalvo, Chiara Saponaro, Maria Moreno-Lopez, Sana Douffi, Abdelkrim El Karchaoui, Gianni Pasquetti, Julien Thevenet, Nathalie Delalleau, Valery Gmyr, Paolo Giacobini, Stéphanie Espiard, Julie Kerr-Conte, François Pattou, Adrian Liston, Caroline Bonner","doi":"10.1172/jci.insight.198095","DOIUrl":"https://doi.org/10.1172/jci.insight.198095","url":null,"abstract":"HNF1A-MODY, the most common monogenic diabetes, exhibits progressive β cell dysfunction, but existing mouse models fail to recapitulate human disease progression, limiting understanding of pathogenic mechanisms. We developed mice with heterozygous deletion of the Hnf1a transactivation domain (Hnf1a+/Δe4-10) to model human HNF1A haploinsufficiency, conducted cross-sectional metabolic characterization, and validated our findings in HNF1A-deficient human islets. Unlike previous models, Hnf1a+/Δe4-10 mice successfully recapitulated temporal HNF1A-MODY progression. Male mice developed sequential pathophysiology: early insulin resistance in young adults (7 weeks), followed by testosterone deficiency and fasting hyperglycemia in adult mice (10 weeks). Glucose intolerance emerged in middle-aged mice (30 weeks), progressing to multi-organ dysfunction in aged mice (44-70 weeks), characterized by elevated hepatic gluconeogenesis, impaired renal glucose handling, and hepatic steatosis/fibrosis. This dual pathophysiology involving β cell dysfunction and peripheral insulin resistance was associated with dysregulated hormone secretion from both α and β cells in aged mice (40-70 weeks). Human islet studies with HNF1A knockdown confirmed translational relevance, demonstrating reduced SGLT2 protein expression and inappropriate glucagon and insulin secretion. This work established a physiologically relevant HNF1A-MODY model, identified early insulin resistance as a key mechanism triggering hormonal dysfunction, and revealed HNF1A's role in multi-organ pathophysiology beyond traditional β cell dysfunction.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Computational identification of migrating T cells in spatial transcriptomics data. 空间转录组学数据中迁移T细胞的计算鉴定。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.192718

Lin Zhong, Bo Li, Zhikai Chi, Siyuan Zhang, Qiwei Li, Guanghua Xiao

{"title":"Computational identification of migrating T cells in spatial transcriptomics data.","authors":"Lin Zhong, Bo Li, Zhikai Chi, Siyuan Zhang, Qiwei Li, Guanghua Xiao","doi":"10.1172/jci.insight.192718","DOIUrl":"https://doi.org/10.1172/jci.insight.192718","url":null,"abstract":"T cells are the central players in antitumor immunity, and effective tumor killing depends on their ability to infiltrate into the tumor microenvironment (TME) while maintaining normal cytotoxicity. However, late-stage tumors develop immunosuppressive mechanisms that impede T cell movement and induce exhaustion. Investigating T cell migration in human tumors in vivo could provide insights into tumor immune escape, although it remains a challenging task. In this study, we developed ReMiTT, a computational method that leverages spatial transcriptomics data to track T cell migration patterns within tumor tissue. Applying ReMiTT to multiple tumor samples, we identified potential migration trails. On these trails, chemokines that promote T cell trafficking displayed an increasing trend. Additionally, we identified key genes and pathways enriched on these migration trails, including those involved in cytoskeleton rearrangement, leukocyte chemotaxis, cell adhesion, leukocyte migration, and extracellular matrix remodeling. Furthermore, we characterized the phenotypes of T cells along these trails, showing that the migrating T cells are highly proliferative. Our findings introduce an approach for studying T cell migration and interactions within the TME, offering valuable insights into tumor-immune dynamics.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A nutrient-responsive AMPK/TBK1 circuit restricts adipocyte catabolism. 营养反应性AMPK/TBK1回路限制脂肪细胞分解代谢。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.200168

Churaibhon Wisessaowapak, Yuliya Skorobogatko, Hyeonhui Kim, Xue Feng, Seunghwan Son, Haipeng Fu, Sitao Zhang, Pichaya Lertvilai, Lina Chang, Annie Hoang, Hetty Chen, Sarah Bedsted, Joseph Valentine, Jin Young Huh, Peng Zhao, Shannon M Reilly, Piyajit Watcharasit, Maryam Ahmadian, Alan R Saltiel

{"title":"A nutrient-responsive AMPK/TBK1 circuit restricts adipocyte catabolism.","authors":"Churaibhon Wisessaowapak, Yuliya Skorobogatko, Hyeonhui Kim, Xue Feng, Seunghwan Son, Haipeng Fu, Sitao Zhang, Pichaya Lertvilai, Lina Chang, Annie Hoang, Hetty Chen, Sarah Bedsted, Joseph Valentine, Jin Young Huh, Peng Zhao, Shannon M Reilly, Piyajit Watcharasit, Maryam Ahmadian, Alan R Saltiel","doi":"10.1172/jci.insight.200168","DOIUrl":"https://doi.org/10.1172/jci.insight.200168","url":null,"abstract":"Metabolic adaptation to both caloric excess and restriction promotes energy conservation by suppressing catabolic pathways via feedback mechanisms that remain incompletely defined. We identified TANK binding kinase 1 (TBK1) as a nutrient- and inflammation-responsive brake on AMPK signaling in adipocytes. Fasting or pharmacological AMPK activation induced Tbk1 transcription via a PGC1α/nuclear respiratory factor 1 axis, which, in turn, limited AMPK activity through a phosphorylation cascade to conserve energy. In obesity, this AMPK/TBK1 axis was disrupted due to chronically elevated basal TBK1, thereby restricting energy expenditure during fasting. Adipocyte-specific TBK1 deletion enhanced fasting-induced AMPK activation, mitochondrial function, and lipolytic gene expression in both lean and obese mice. Pharmacological TBK1 inhibition with amlexanox recapitulated these effects. Combined treatment of mice with amlexanox and the AMPK activator AICAR enhanced weight loss, improved glucose tolerance and insulin sensitivity, and suppressed inflammatory and lipogenic programs in adipose tissue, as well as fibrotic gene expression in the liver. Building on prior clinical observations linking TBK1 inhibition to metabolic health, these findings defined a nutrient-sensitive AMPK/TBK1 feedback loop that limited adipocyte catabolism and suggested that dual targeting of TBK1 and AMPK may help counteract metabolic adaptation and enhance the durability of obesity therapies.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Negative regulation of human IL-33 in endothelium during allergic airway inflammation. 人IL-33在变应性气道炎症中的负调控作用。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.190418

Maile K Hollinger, Chanie L Howard, Donna C Decker, Kelly M Blaine, Ivy Aneas, Emily M Grayson, Tania E Velez, Fernando A Oliveira, Riley T Hannan, Daniel F Camacho, Philip A Verhoef, Cara L Hrusch, Rebecca S Griffes, Jeffrey M Sturek, Marcelo A Nobrega, Nathan Schoettler, Anne I Sperling

{"title":"Negative regulation of human IL-33 in endothelium during allergic airway inflammation.","authors":"Maile K Hollinger, Chanie L Howard, Donna C Decker, Kelly M Blaine, Ivy Aneas, Emily M Grayson, Tania E Velez, Fernando A Oliveira, Riley T Hannan, Daniel F Camacho, Philip A Verhoef, Cara L Hrusch, Rebecca S Griffes, Jeffrey M Sturek, Marcelo A Nobrega, Nathan Schoettler, Anne I Sperling","doi":"10.1172/jci.insight.190418","DOIUrl":"https://doi.org/10.1172/jci.insight.190418","url":null,"abstract":"Lung IL-33 is involved in pathogen defense, barrier homeostasis, and development of allergic responses. We previously identified a 5 kb noncoding region within a GWAS-defined segment that regulates expression of human IL33 (hIL33) but is absent in the murine locus. To understand how this region affects IL-33 expression in vivo, we engineered 2 BAC-transgenic strains in which 166 kb of the human genome upstream of the hIL33 locus, along with a fluorescent reporter, was inserted into the murine genome, both with and without the 5 kb region. Comparison to a murine Il33 (mIl33) reporter strain revealed species-specific tropism; hIL33 reporter was mostly expressed in the endothelium, while mIl33 reporter was expressed in type 2 alveolar epithelium. hIL33 reporter expression in tracheal basal epithelium, submucosal glands, and lung microvasculature required the 5 kb region. Surprisingly, allergen and exogenous IL-33 downregulated hIL33 reporter in lung endothelium only when the 5 kb region was present. Similar IL-33-dependent downregulation of IL33 transcripts was observed in human endothelial cell lines, validating that our hIL33 reporter strain recapitulated human endothelial biology. Together, these data reveal the importance of the asthma-associated human 5 kb region in regulating human IL33 expression in a cell type- and context-dependent manner.","PeriodicalId":14722,"journal":{"name":"JCI insight","volume":"11 9","pages":""},"PeriodicalIF":6.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Clonal hematopoiesis in lung adenocarcinoma pathogenesis. 克隆造血在肺腺癌发病机制中的作用。

IF 6.1 1区医学

JCI insight Pub Date : 2026-05-08 DOI: 10.1172/jci.insight.203981

Tiziana Parisi, Blanca Santibanez Ocampo, Jacob Adelman, Yuyan Cai, Marie McConkey, Christopher J Gibson, Benjamin L Ebert, Peter Miller, Tyler Jacks

引用次数: 0

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