Molecular Therapy最新文献_第8页

Turning ON the inner retinal circuity: An exciting new approach to optogenetic therapy.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-02-24 DOI: 10.1016/j.ymthe.2025.02.011

Boris Rosin, Jose-Alain Sahel

引用次数: 0

PBAE-PEG-based lipid nanoparticles for lung cell-specific gene delivery.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-01-25 DOI: 10.1016/j.ymthe.2025.01.037

Bingxin Liu, Yamato Sajiki, Nicole Littlefield, Yongan Hu, William D Stuart, Anusha Sridharan, Xuemei Cui, Matthew E Siefert, Koichi Araki, Assem G Ziady, Donglu Shi, Jeffery A Whitsett, Yutaka Maeda

{"title":"PBAE-PEG-based lipid nanoparticles for lung cell-specific gene delivery.","authors":"Bingxin Liu, Yamato Sajiki, Nicole Littlefield, Yongan Hu, William D Stuart, Anusha Sridharan, Xuemei Cui, Matthew E Siefert, Koichi Araki, Assem G Ziady, Donglu Shi, Jeffery A Whitsett, Yutaka Maeda","doi":"10.1016/j.ymthe.2025.01.037","DOIUrl":"10.1016/j.ymthe.2025.01.037","url":null,"abstract":"Exemplified by successful use in COVID-19 vaccination, delivery of modified mRNA encapsulated in lipid nanoparticles (LNPs) provides a framework for treating various genetic and acquired disorders. However, LNPs that can deliver mRNA into specific lung cell types have not yet been established. Here, we sought to determine whether poly(β-amino ester)s (PBAE) or PEGylated PBAE (PBAE-PEG) in combination with 4A3-SC8/DOPE/cholesterol/DOTAP LNPs could deliver mRNA into different types of lung cells in vivo. PBAE-PEG/LNP was similar to Lipofectamine MessengerMAX followed by PBAE/LNP for mRNA transfection efficiency in HEK293T cells in vitro. PBAE-PEG/LNP administered by intravenous (IV) injection achieved 73% mRNA transfection efficiency into lung endothelial cells, while PBAE-PEG/LNP administered by intratracheal (IT) injection achieved 55% efficiency in lung alveolar type II (ATII) epithelial cells in mice in vivo. PBAE/LNP administered by IT injection were superior for specific delivery into lung airway club epithelial cells compared to PBAE-PEG/LNP. Lipofectamine MessengerMAX was inactive in vivo. 5-Methoxyuridine-modified mRNA was more efficient than unmodified mRNA in vivo but not in vitro. Our findings indicate that PBAE-PEG/LNP and PBAE/LNP can transfect multiple lung cell types in vivo, which can be applied in gene therapy targeting genetic lung diseases.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":"1154-1165"},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

SINEUP RNA rescues molecular phenotypes associated with CHD8 suppression in autism spectrum disorder model systems. 在自闭症谱系障碍模型系统中，sinineup RNA拯救与CHD8抑制相关的分子表型。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2024-12-30 DOI: 10.1016/j.ymthe.2024.12.043

Francesca Di Leva, Michele Arnoldi, Stefania Santarelli, Mathieu Massonot, Marianne Victoria Lemée, Carlotta Bon, Miguel Pellegrini, Maria Elena Castellini, Giulia Zarantonello, Andrea Messina, Yuri Bozzi, Raphael Bernier, Silvia Zucchelli, Simona Casarosa, Erik Dassi, Giuseppe Ronzitti, Christelle Golzio, Jasmin Morandell, Stefano Gustincich, Stefano Espinoza, Marta Biagioli

{"title":"SINEUP RNA rescues molecular phenotypes associated with CHD8 suppression in autism spectrum disorder model systems.","authors":"Francesca Di Leva, Michele Arnoldi, Stefania Santarelli, Mathieu Massonot, Marianne Victoria Lemée, Carlotta Bon, Miguel Pellegrini, Maria Elena Castellini, Giulia Zarantonello, Andrea Messina, Yuri Bozzi, Raphael Bernier, Silvia Zucchelli, Simona Casarosa, Erik Dassi, Giuseppe Ronzitti, Christelle Golzio, Jasmin Morandell, Stefano Gustincich, Stefano Espinoza, Marta Biagioli","doi":"10.1016/j.ymthe.2024.12.043","DOIUrl":"10.1016/j.ymthe.2024.12.043","url":null,"abstract":"Loss-of-function mutations in the chromodomain helicase DNA-binding 8 (CHD8) gene are strongly associated with autism spectrum disorders (ASDs). Indeed, the reduction of CHD8 causes transcriptional, epigenetic, and cellular phenotypic changes correlated to disease, which can be monitored in assessing new therapeutic approaches. SINEUPs are a functional class of natural and synthetic antisense long non-coding RNAs able to stimulate the translation of sense target mRNA, with no effect on transcription. Here, we employed synthetic SINEUP-CHD8 targeting the first and third AUG of the CHD8 coding sequence to efficiently stimulate endogenous CHD8 protein production. SINEUP-CHD8 were effective in cells with reduced levels of the target protein and in patient-derived fibroblasts with CHD8 mutations. Functionally, SINEUP-CHD8 were able to revert molecular phenotypes associated with CHD8 suppression, i.e., genome-wide transcriptional dysregulation, and the reduction of H3K36me3 levels. Strikingly, in chd8-morpholino-treated and ENU mutant zebrafish embryos, SINEUP-chd8 injection confirmed the ability of SINEUP RNA to rescue the chd8-suppression-induced macrocephaly phenotype and neuronal hyperproliferation. Thus, SINEUP-CHD8 molecule(s) represent a proof-of-concept toward the development of an RNA-based therapy for neurodevelopmental syndromes with implications for, and beyond ASD, and relevant to genetic disorders caused by protein haploinsufficiency.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":"1180-1196"},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

TRAF1 promotes osteoclastogenesis by enhancing metabolic adaptation to oxidative phosphorylation in an AKT-dependent manner. TRAF1 以 AKT 依赖性方式增强氧化磷酸化的代谢适应性，从而促进破骨细胞生成。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-01-25 DOI: 10.1016/j.ymthe.2025.01.040

Honglei Kang, Renpeng Peng, Yimin Dong, Fuben Liao, Meipeng Zhu, Pengju Wang, Shi-An Hu, Peixuan Hu, Jia Wang, Zheming Liu, Kehan Song, Feng Li

{"title":"TRAF1 promotes osteoclastogenesis by enhancing metabolic adaptation to oxidative phosphorylation in an AKT-dependent manner.","authors":"Honglei Kang, Renpeng Peng, Yimin Dong, Fuben Liao, Meipeng Zhu, Pengju Wang, Shi-An Hu, Peixuan Hu, Jia Wang, Zheming Liu, Kehan Song, Feng Li","doi":"10.1016/j.ymthe.2025.01.040","DOIUrl":"10.1016/j.ymthe.2025.01.040","url":null,"abstract":"Tumor necrosis factor receptor-associated factor 1 (TRAF1) is a crucial signaling adaptor involved in multiple cellular events. However, its role in regulating osteoclastogenesis and energy metabolism remains unclear. Here, we report that TRAF1 promotes osteoclastogenesis and oxidative phosphorylation (OXPHOS). Employing RNA sequencing, we found that TRAF1 is markedly upregulated during osteoclastogenesis and is positively associated with osteoporosis. TRAF1 knockout inhibits osteoclastogenesis and increases bone mass in both normal and ovariectomized adult mice without affecting bone mass in childhood. Furthermore, TRAF1 promotes osteoclast OXPHOS by increasing the phosphorylation level of AKT. Mechanistically, TRAF1 functions to inhibit TRAF2-induced ubiquitination of Gβl, a known activator of AKT, and further upregulates AKT phosphorylation. Rescue experiments revealed that the inhibitory effects of TRAF1 knockout on osteoclastogenesis, OXPHOS, and bone mass are dependent on AKT. Collectively, our findings uncover a previously unrecognized function of TRAF1 in regulating osteoclastogenesis and energy metabolism, and establish a novel TRAF1-AKT-OXPHOS axis in osteoclasts.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":"933-949"},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143040300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Retraction Notice to: ESCRT-mediated Uptake and Degradation of Brain-targeted α-synuclein Single Chain Antibody Attenuates Neuronal Degeneration In Vivo.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-02-02 DOI: 10.1016/j.ymthe.2025.01.027

Brian Spencer, Sharareh Emadi, Paula Desplats, Simona Eleuteri, Sarah Michael, Kori Kosberg, Jay Shen, Edward Rockenstein, Christina Patrick, Anthony Adame, Tania Gonzalez, Michael Sierks, Eliezer Masliah

引用次数: 0

FKBP51 inhibition ameliorates neurodegeneration and motor dysfunction in the neuromelanin-SNCA mouse model of Parkinson's disease.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-02-03 DOI: 10.1016/j.ymthe.2025.01.049

Marta Garcia-Gomara, Naroa Legarra-Marcos, Maria Serena, Elvira Rojas-de-Miguel, Maria Espelosin, Irene Marcilla, Alberto Perez-Mediavilla, Maria Rosario Luquin, Jose Luis Lanciego, Maria Angeles Burrell, Mar Cuadrado-Tejedor, Ana Garcia-Osta

{"title":"FKBP51 inhibition ameliorates neurodegeneration and motor dysfunction in the neuromelanin-SNCA mouse model of Parkinson's disease.","authors":"Marta Garcia-Gomara, Naroa Legarra-Marcos, Maria Serena, Elvira Rojas-de-Miguel, Maria Espelosin, Irene Marcilla, Alberto Perez-Mediavilla, Maria Rosario Luquin, Jose Luis Lanciego, Maria Angeles Burrell, Mar Cuadrado-Tejedor, Ana Garcia-Osta","doi":"10.1016/j.ymthe.2025.01.049","DOIUrl":"10.1016/j.ymthe.2025.01.049","url":null,"abstract":"Parkinson's disease (PD) is characterized by the loss of neuromelanin (NM)-containing dopaminergic (DA) neurons in the substantia nigra (SN) pars compacta (SNpc) and the buildup of α-synuclein (α-syn) inclusions, called Lewy bodies. To investigate the roles of NM and α-syn in DA neuron degeneration, we modeled PD by inducing NM accumulation in a humanized α-syn mouse model (Snca-; PAC-Tg(SNCAWT)) via the expression of human tyrosinase in the SN. We found that this mouse strain develops naturally progressive motor dysfunction and dopaminergic neuronal loss in the SN with aging. Upon tyrosinase injection, NM-containing neurons developed p62 and ubiquitin inclusions. Furthermore, the upregulation of genes associated with microglial activation in the midbrain indicated a role of pro-inflammatory factors in neurodegeneration. Midbrain RNA sequencing confirmed the microglial response and identified Fkbp5 as one of the more dysregulated genes. Next, we showed that FKBP51(51 kDa) was significantly upregulated with aging and in PD human brains. Pharmacological treatment with SAFit2, a potent FKBP51 inhibitor, led to a reduction in ubiquitin-positive inclusions, prevention of neurodegeneration in the SNpc, and improved motor function in NM-SNCAWT mice. These results highlight the critical role of FKBP51 in PD and propose SAFit2 as a promising therapeutic candidate for reducing neurodegeneration in PD.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":"895-916"},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143190038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Gene editing of CD3 epsilon to redirect regulatory T cells for adoptive T cell transfer. 对 CD3 epsilon 基因进行基因编辑，以重定向调节性 T 细胞，实现收养性 T 细胞转移。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-02-03 DOI: 10.1016/j.ymthe.2025.01.045

Weijie Du, Fatih Noyan, Oliver McCallion, Vanessa Drosdek, Jonas Kath, Viktor Glaser, Carla Fuster-Garcia, Mingxing Yang, Maik Stein, Clemens Franke, Yaolin Pu, Olaf Weber, Julia K Polansky, Toni Cathomen, Elmar Jaeckel, Joanna Hester, Fadi Issa, Hans-Dieter Volk, Michael Schmueck-Henneresse, Petra Reinke, Dimitrios L Wagner

{"title":"Gene editing of CD3 epsilon to redirect regulatory T cells for adoptive T cell transfer.","authors":"Weijie Du, Fatih Noyan, Oliver McCallion, Vanessa Drosdek, Jonas Kath, Viktor Glaser, Carla Fuster-Garcia, Mingxing Yang, Maik Stein, Clemens Franke, Yaolin Pu, Olaf Weber, Julia K Polansky, Toni Cathomen, Elmar Jaeckel, Joanna Hester, Fadi Issa, Hans-Dieter Volk, Michael Schmueck-Henneresse, Petra Reinke, Dimitrios L Wagner","doi":"10.1016/j.ymthe.2025.01.045","DOIUrl":"10.1016/j.ymthe.2025.01.045","url":null,"abstract":"Adoptive transfer of antigen-specific regulatory T cells (Tregs) is a promising strategy to combat immunopathologies in transplantation and autoimmune diseases. However, their low frequency in peripheral blood poses challenges for both manufacturing and clinical application. Chimeric antigen receptors have been used to redirect the specificity of Tregs, using retroviral vectors. However, retroviral gene transfer is costly, time consuming, and raises safety issues. Here, we explored non-viral CRISPR-Cas12a gene editing to redirect Tregs, using human leukocyte antigen (HLA)-A2-specific constructs for proof-of-concept studies in transplantation models. Knock-in of an antigen-binding domain into the N terminus of CD3 epsilon (CD3ε) gene generates Tregs expressing a chimeric CD3ε-T cell receptor fusion construct (TRuC) protein that integrates into the endogenous TCR/CD3 complex. These CD3ε-TRuC Tregs exhibit potent antigen-dependent activation while maintaining responsiveness to TCR/CD3 stimulation. This enables preferential enrichment of TRuC-redirected Tregs over CD3ε knockout Tregs via repetitive CD3/CD28 stimulation in a good manufacturing practice-compatible expansion system. CD3ε-TRuC Tregs retained their phenotypic, epigenetic, and functional identity. In a humanized mouse model, HLA-A2-specific CD3ε-TRuC Tregs demonstrate superior protection of allogeneic HLA-A2+ skin grafts from rejection compared with polyclonal Tregs. This approach provides a pathway for developing clinical-grade CD3ε-TRuC-based Treg cell products for transplantation immunotherapy and other immunopathologies.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":"997-1013"},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143190042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Focused-ultrasound-mediated CRISPR-Cas9 gene editing in human induced pluripotent stem cells.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-02-20 DOI: 10.1016/j.ymthe.2025.02.006

Bernie Simone Owusu-Yaw

引用次数: 0

Clinical applications of oligonucleotides for cancer therapy.

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 DOI: 10.1016/j.ymthe.2025.02.045

Vittorio DeFranciscis, Giovanni Amabile, Marcin Kortylewski

{"title":"Clinical applications of oligonucleotides for cancer therapy.","authors":"Vittorio DeFranciscis, Giovanni Amabile, Marcin Kortylewski","doi":"10.1016/j.ymthe.2025.02.045","DOIUrl":"10.1016/j.ymthe.2025.02.045","url":null,"abstract":"Oligonucleotide therapeutics (ONTs) represent a rapidly evolving modality for cancer treatment, capitalizing on their ability to modulate gene expression with high specificity. With more than 20 nucleic acid-based therapies that gained regulatory approval, advances in chemical modifications, sequence optimization, and novel delivery systems have propelled ONTs from research tools to clinical realities. ONTs, including siRNAs, antisense oligonucleotides, saRNA, miRNA, aptamers, and decoys, offer promising solutions for targeting previously \"undruggable\" molecules, such as transcription factors, and enhancing cancer immunotherapy by overcoming tumor immune evasion. The promise of ONT application in cancer treatment is exemplified by the recent FDA approval of the first oligonucleotide-based treatment to myeloproliferative disease. At the same time, there are challenges in delivering ONTs to specific tissues, mitigating off-target effects, and improving cellular uptake and endosomal release. This review provides a comprehensive overview of ONTs in clinical trials, emerging delivery strategies, and innovative therapeutic approaches, emphasizing the role of ONTs in immunotherapy and addressing hurdles that hinder their clinical translation. By examining advances and remaining challenges, we highlight opportunities for ONTs to revolutionize oncology and enhance patient outcomes.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":""},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567755","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

Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease. 玻璃体连接蛋白调节慢性阻塞性肺疾病的肺组织重塑和肺气肿。

IF 12.1 1区医学

Molecular Therapy Pub Date : 2025-03-05 Epub Date: 2025-01-21 DOI: 10.1016/j.ymthe.2025.01.032

Gang Liu, Alan C Hsu, Silke Geirnaert, Christine Cong, Prema M Nair, Sj Shen, Jacqueline E Marshall, Tatt Jhong Haw, Michael Fricker, Ashleigh M Philp, Nicole G Hansbro, Stelios Pavlidis, Yike Guo, Janette K Burgess, Leandro Castellano, Antonio Ieni, Gaetano Caramori, Brain G G Oliver, K Fan Chung, Ian M Adcock, Darryl A Knight, Francesca Polverino, Ken Bracke, Peter A Wark, Philip M Hansbro

{"title":"Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.","authors":"Gang Liu, Alan C Hsu, Silke Geirnaert, Christine Cong, Prema M Nair, Sj Shen, Jacqueline E Marshall, Tatt Jhong Haw, Michael Fricker, Ashleigh M Philp, Nicole G Hansbro, Stelios Pavlidis, Yike Guo, Janette K Burgess, Leandro Castellano, Antonio Ieni, Gaetano Caramori, Brain G G Oliver, K Fan Chung, Ian M Adcock, Darryl A Knight, Francesca Polverino, Ken Bracke, Peter A Wark, Philip M Hansbro","doi":"10.1016/j.ymthe.2025.01.032","DOIUrl":"10.1016/j.ymthe.2025.01.032","url":null,"abstract":"Vitronectin (VTN) is an important extracellular matrix protein in tissue remodeling, but its role in chronic obstructive pulmonary disease (COPD) is unknown. We show that VTN regulates tissue remodeling through urokinase plasminogen activator (uPA) signaling pathway in COPD. In human COPD airways and bronchoepithelial cells and the airways of mice with cigarette smoke (CS)-induced experimental COPD, VTN protein was not changed, but downstream uPA signaling was altered (increased plasminogen activator inhibitor-1) that induced collagen and airway remodeling. In the parenchyma, VTN levels were decreased, uPA signaling pathway differentially altered and collagen reduced in lung fibroblasts from human and lung parenchyma in experimental COPD. Vtn inhibition with siRNA in mouse fibroblasts altered uPA signaling increased matrix metalloproteinase-12, and reduced collagen, whereas over-expression restored collagen production after CS extract challenge. Vtn-/- and Vtn small interfering RNA-treated mice had exaggerated inflammation, emphysema, and impaired lung function compared with controls with CS-induced COPD. Restoration of VTN in the parenchyma may be a therapeutic option for emphysema and COPD.","PeriodicalId":19020,"journal":{"name":"Molecular Therapy","volume":" ","pages":"917-932"},"PeriodicalIF":12.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143007659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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