Molecular biomedicine最新文献

{"title":"Metastasis-associated lung adenocarcinoma transcript 1 overexpression in testis contributes to idiopathic non-obstructive azoospermia via repressing ETS variant transcription factor 5.","authors":"Lei Wei, Zonggang Feng, Qian Dou, Pengfen Li, Xinghua Zhao, Bin Hao","doi":"10.1186/s43556-024-00235-6","DOIUrl":"10.1186/s43556-024-00235-6","url":null,"abstract":"<p><p>Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), is a long non-coding RNA localized in the cell nucleus, known for its multifunctional roles, including potential involvement in spermatogenesis. This study investigates the mechanism by which MALAT1 dysregulation contributes to the pathogenesis of idiopathic non-obstructive azoospermia (iNOA). We analyzed MALAT1 levels in two gene expression profiling datasets comprising patients with obstructive azoospermia (OA) who have normal spermatogenesis and 13 patients with iNOA. The dysregulation of MALAT1 along with the expression levels of its negatively correlated genes were confirmed in a larger cohort of 24 OA patients and 38 iNOA patients. We examined the effects of MALAT1 overexpression in primary human spermatogonial stem cells (SSCs) and Sertoli cells. Additionally, we assessed DNA methylation, as well as levels of H3K27me3 and H3K27Ac level near the etv5 promoter region using ChIP-qPCR. We observed that MALAT1 was overexpressed in testes of iNOA patients with its levels negatively correlating with six spermatogenesis related genes and positively correlated with three others. Overexpression of MALAT1 in SSCs repressed proliferation and induced apoptosis while also suppressing ETS variant transcription factor 5 (ETV5) expression by promoting H3K27 tri-methylation of the ETV5 promoter. Overexpression of MALAT1 in Sertoli cells did not induce apoptosis but impaired their cell supporting function. In conclusion, MALAT1 overexpression in SSCs contributes to the pathogenesis of iNOA via downregulating ETV5 expression and promoting cell apoptosis.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"71"},"PeriodicalIF":6.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11649603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142840491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer-associated fibroblasts: heterogeneity, tumorigenicity and therapeutic targets.","authors":"Keke Lv, Tianlin He","doi":"10.1186/s43556-024-00233-8","DOIUrl":"10.1186/s43556-024-00233-8","url":null,"abstract":"<p><p>Cancer, characterized by its immune evasion, active metabolism, and heightened proliferation, comprises both stroma and cells. Although the research has always focused on parenchymal cells, the non-parenchymal components must not be overlooked. Targeting cancer parenchymal cells has proven to be a formidable challenge, yielding limited success on a broad scale. The tumor microenvironment(TME), a critical niche for cancer cell survival, presents a novel way for cancer treatment. Cancer-associated fibroblast (CAF), as a main component of TME, is a dynamically evolving, dual-functioning stromal cell. Furthermore, their biological activities span the entire spectrum of tumor development, metastasis, drug resistance, and prognosis. A thorough understanding of CAFs functions and therapeutic advances holds significant clinical implications. In this review, we underscore the heterogeneity of CAFs by elaborating on their origins, types and function. Most importantly, by elucidating the direct or indirect crosstalk between CAFs and immune cells, the extracellular matrix, and cancer cells, we emphasize the tumorigenicity of CAFs in cancer. Finally, we highlight the challenges encountered in the exploration of CAFs and list targeted therapies for CAF, which have implications for clinical treatment.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"70"},"PeriodicalIF":6.3,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11649616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircMYH9/miR-133a-3p/CXCR4 axis: a novel regulatory network in sperm fertilization and embryo development.","authors":"Qian Sun, Yanyu Li, Wen Yang, Wen Feng, Jiayun Zhou, Yijuan Cao, Bei Zhang, Zuobin Zhu, Conghui Han","doi":"10.1186/s43556-024-00236-5","DOIUrl":"10.1186/s43556-024-00236-5","url":null,"abstract":"<p><p>This study aimed to investigate the influence of sperm miRNAs on fertilization rates (FR) in in vitro fertilization (IVF) and to explore potential regulatory mechanisms in sperm-mediated fertilization and embryo development. Through high-throughput sequencing, we identified differentially expressed miRNAs in sperm, with miR-133a-3p significantly upregulated in samples associated with low FR and available embryo rate (AER). Key regulatory circRNAs and mRNAs were further identified via the Starbase database, intersected with differentially expressed RNA, and analyzed through GO, KEGG, and PPI analyses. The circMYH9/miR-133a-3p/CXCR4 axis emerged as a critical regulatory network. In vitro assays using the GC-2 spd mouse spermatogenic cell line revealed that miR-133a-3p inhibited cell growth and proliferation while promoting apoptosis. circMYH9, acting as a competing endogenous RNA (ceRNA) for miR-133a-3p, modulated CXCR4 expression, enhancing GC-2 spd cell growth and inhibiting apoptosis through the miR-133a-3p/CXCR4 axis. In vivo experiments using a mouse model confirmed that circMYH9 overexpression increased IVF success rates and promoted embryo development via this axis. Mechanistically, miR-133a-3p suppresses sperm fertilization and embryo development by targeting the circMYH9/miR-133a-3p/CXCR4 axis. These findings suggest that this regulatory network could serve as a novel biomarker for assessing fertilization potential and embryo quality in clinical settings and as a potential therapeutic target to improve IVF outcomes and address infertility. This study provides valuable insights into the molecular mechanisms governing sperm function and early embryonic development.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"69"},"PeriodicalIF":6.3,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11645365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142820315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pentraxin-3 modulates hepatocyte ferroptosis and the innate immune response in LPS-induced liver injury.","authors":"Huitong Wang, Zhaojie Su, Yunyun Qian, Baojie Shi, Hao Li, Wenbin An, Yi Xiao, Cheng Qiu, Zhixiang Guo, Jianfa Zhong, Xia Wu, Jiajia Chen, Ying Wang, Wei Zeng, Linghui Zhan, Jie Wang","doi":"10.1186/s43556-024-00227-6","DOIUrl":"10.1186/s43556-024-00227-6","url":null,"abstract":"<p><p>The liver plays a crucial role in the immune response during endotoxemia and is one of the critical targets for sepsis-related injuries. As a secretory factor involved in inflammation, pentraxin-3 (PTX3) has been demonstrated to regulate hepatic homeostasis; however, the relationship between PTX3 and cell crosstalk between immune cells and hepatocytes in the liver remains incompletely understood. In this study, we revealed that, compared with WT mice, Ptx3^-/- mice with lipopolysaccharide (LPS)-induced endotoxemia exhibited alleviated liver damage, with reduced serum alanine transaminase and aspartate transaminase levels and an improved survival rate. Mechanistically, RNA-Seq and western blot results revealed that Ptx3 knockdown in hepatocytes increased the expression of Tfrc and Ccl20; consequently, Ptx3 deficiency regulated LPS-induced hepatocyte ferroptosis via increased mitochondrial reactive oxygen species and Fe²⁺ and recruited more macrophages by CCL20/CCR6 axis to be involved in inflammation and the clearance of harmful substances. Moreover, western blot and immunofluorescence staining confirmed that the NF-κB signaling pathway was upregulated upon LPS treatment in Ptx3-knockdown macrophages, promoting phagocytosis and polarization toward M1 macrophages. Collectively, our findings show that the absence of Ptx3 can ameliorate sepsis-induced liver injury by regulating hepatocyte ferroptosis and promote the recruitment and polarization of M1 macrophages. These findings offer a key basis for the development of effective treatments for acute infections.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"68"},"PeriodicalIF":6.3,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11638432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acetyltransferase NAT10 promotes an immunosuppressive microenvironment by modulating CD8⁺ T cell activity in prostate cancer.","authors":"Ji Liu, Zhuoran Gu, Libin Zou, Zhijin Zhang, Liliang Shen, Ruiliang Wang, Shaobo Xue, Jiang Geng, Shiyu Mao, Wentao Zhang, Xudong Yao","doi":"10.1186/s43556-024-00228-5","DOIUrl":"10.1186/s43556-024-00228-5","url":null,"abstract":"<p><p>N-acetyltransferase 10 (NAT10), an enzyme responsible for ac4C acetylation, is implicated in cancer progression, though its specific biological function in prostate cancer remains insufficiently understood. This study clarifies NAT10's role in prostate cancer and its effects on the tumor immune microenvironment. NAT10 expression and clinical relevance were assessed through bioinformatics, RT-qPCR, and IHC analyses, comparing prostate cancer tissues with normal controls. The impact of NAT10 on tumor cell proliferation, migration, and invasion was investigated via in vitro assays-including CCK-8, EdU, wound healing, and 3D-Transwell-as well as in vivo mouse xenograft models and organoid studies. Further, NAT10's influence on immune cell infiltration was examined using flow cytometry, IHC, cell co-culture assays, and ELISA to elucidate downstream chemokine effects, specifically targeting CD8⁺ T cells. Findings indicated significant upregulation of NAT10 in prostate cancer cells, enhancing their proliferative and invasive capacities. Notably, NAT10 suppresses CD8⁺ T cell recruitment and cytotoxicity through the CCL25/CCR9 axis, fostering an immunosuppressive microenvironment that exacerbates tumor progression. An ac4C modification score was also devised based on NAT10's downstream targets, providing a novel predictive tool for evaluating immune infiltration and forecasting immunotherapy responses in patients with prostate cancer. This study underscores NAT10's pivotal role in modulating the prostate cancer immune microenvironment, offering insights into the immune desert phenomenon and identifying NAT10 as a promising therapeutic target for improving immunotherapy efficacy.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"67"},"PeriodicalIF":6.3,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11625704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptome profiling of m⁶A regulator-mediated methylation modification patterns in elderly acute myeloid leukemia patients.","authors":"Zhe Wang, Xin Du, Peidong Zhang, Meiling Zhao, Tianbo Zhang, Jiang Liu, Xiaolan Wang, Doudou Chang, Xiaxia Liu, Sicheng Bian, Xialin Zhang, Ruijuan Zhang","doi":"10.1186/s43556-024-00234-7","DOIUrl":"10.1186/s43556-024-00234-7","url":null,"abstract":"<p><p>Millions of people worldwide die of acute myeloid leukaemia (AML) each year. Although N6-methyladenosine (m⁶A) modification has been reported to regulate the pathogenicity of AML, the mechanisms by which m⁶A induces dysfunctional hematopoietic differentiation in elderly AML patients remain elusive. This study elucidates the mechanisms of the m⁶A landscape and the specific roles of m⁶A regulators in hematopoietic cells of elderly AML patients. Notably, fat mass and obesity-associated protein (FTO) was found to be upregulated in hematopoietic stem cells (HSCs), myeloid cells, and T-cells, where it inhibits their differentiation via the WNT signaling pathway. Additionally, elevated YT521-B homology domain family proteins 2 (YTHDF2) expression in erythrocytes was observed to negatively regulate differentiation through oxidative phosphorylation, resulting in leukocyte activation. Moreover, IGF2BP2 was significantly upregulated in myeloid cells, contributing to an aberrant chromosomal region and disrupted oxidative phosphorylation. m⁶A regulators were shown to induce abnormal cell-cell communication within hematopoietic cells, mediating ligand-receptor interactions across various cell types through the HMGB1-mediated pathway, thereby promoting AML progression. External validation was conducted using an independent single-cell RNA sequencing (scRNA-Seq) dataset. The THP-1 and MV411 cell lines were utilized to corroborate the m⁶A regulator profile; in vitro experiments involving short hairpin RNA (shRNA) targeting FTO demonstrated inhibition of cell proliferation, migration, and oxidative phosphorylation, alongside induction of cell cycle arrest and apoptosis. In summary, these findings suggest that the upregulation of m⁶A regulators in HSCs, erythrocytes, myeloid cells, and T-cells may contribute to the malignant differentiation observed in AML patients. This research provides novel insights into the pathogenesis of AML in elderly patients and identifies potential therapeutic targets.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"66"},"PeriodicalIF":6.3,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11624184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142788033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characteristics of the early innate response induced by the aerosolized Ad5-vectored COVID-19 vaccine.","authors":"Wan-Ru Zheng, Jun-Yan Dan, Nan Huo, Zhe Zhang, Li-Hua Hou","doi":"10.1186/s43556-024-00232-9","DOIUrl":"10.1186/s43556-024-00232-9","url":null,"abstract":"","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"64"},"PeriodicalIF":6.3,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142781818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycosyltransferase B4GALNT1 promotes immunosuppression in hepatocellular carcinoma via the HES4-SPP1-TAM/Th2 axis.","authors":"Zhifeng Wang, Jiaxin Liu, Xiaoming Wang, Qingyun Wu, Qiao Peng, Tianxiao Yang, Xuehui Sun, Xiaofeng Wang, Yilin Wang, Weicheng Wu","doi":"10.1186/s43556-024-00231-w","DOIUrl":"10.1186/s43556-024-00231-w","url":null,"abstract":"<p><p>β-1,4-N-acetylgalactosaminyltransferase I (B4GALNT1) is a key glycosyltransferase for gangliosides. Its aberrant expression has been observed in various cancers, and its potential roles in tumor immunity were suggested recently. However, how B4GALNT1 regulate tumor progression and tumor immunity remains largely unknown. In this study, we aimed to investigate the roles of B4GALNT1 in hepatocellular carcinoma (HCC), particularly in reshaping the tumor immune microenvironment, and evaluate the potential beneficial effects of targeting B4GALNT1 in immunotherapy. Our data verified the aberrant upregulation of B4GALNT1 in HCC tumor tissues and tumor cells, which could be utilized as an independent prognostic factor and improve the predicting performance of traditional tumor node metastasis (TNM) system. We also demonstrated that B4GALNT1 increased the phosphorylation of Hes Family BHLH Transcription Factor 4 (HES4) via p38 mitogen-activated protein kinase (p38)/ c-Jun N-terminal kinase (JNK) signaling in tumor cells, thus increasing the transcriptional activity of HES4, which upregulated the synthesis and secretion of secreted phosphoprotein 1 (SPP1), modulated the composition of tumor-associated macrophages (TAMs) and T helper type 2 (Th2) cells, and eventually reshaped the immunosuppressive microenvironment. In addition, silencing B4GALNT1 was proved to enhance the tumor-killing efficiency of the programmed cell death protein 1 (PD-1)-targeting strategy in mouse model. In conclusion, this study evaluated B4GALNT1 as a prognostic predictor for HCC patients and revealed the mechanism of B4GALNT1 in microenvironmental remodeling, which extends the understanding of HCC progression and provides a novel auxiliary strategy for HCC immunotherapy.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"65"},"PeriodicalIF":6.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142775269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor energy metabolism: implications for therapeutic targets.","authors":"Youwu Hu, Wanqing Liu, WanDi Fang, Yudi Dong, Hong Zhang, Qing Luo","doi":"10.1186/s43556-024-00229-4","DOIUrl":"10.1186/s43556-024-00229-4","url":null,"abstract":"<p><p>Tumor energy metabolism plays a crucial role in the occurrence, progression, and drug resistance of tumors. The study of tumor energy metabolism has gradually become an emerging field of tumor treatment. Recent studies have shown that epigenetic regulation is closely linked to tumor energy metabolism, influencing the metabolic remodeling and biological traits of tumor cells. This review focuses on the primary pathways of tumor energy metabolism and explores therapeutic strategies to target these pathways. It covers key areas such as glycolysis, the Warburg effect, mitochondrial function, oxidative phosphorylation, and the metabolic adaptability of tumors. Additionally, this article examines the role of the epigenetic regulator SWI/SNF complex in tumor metabolism, specifically its interactions with glucose, lipids, and amino acids. Summarizing therapeutic strategies aimed at these metabolic pathways, including inhibitors of glycolysis, mitochondrial-targeted drugs, exploitation of metabolic vulnerabilities, and recent developments related to SWI/SNF complexes as potential targets. The clinical significance, challenges, and future directions of tumor metabolism research are discussed, including strategies to overcome drug resistance, the potential of combination therapy, and the application of new technologies.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"63"},"PeriodicalIF":6.3,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11604893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multidrug resistance in Pseudomonas aeruginosa: genetic control mechanisms and therapeutic advances.","authors":"Yuanjing Zhao, Haoran Xu, Hui Wang, Ping Wang, Simin Chen","doi":"10.1186/s43556-024-00221-y","DOIUrl":"10.1186/s43556-024-00221-y","url":null,"abstract":"<p><p>Pseudomonas aeruginosa is a significant opportunistic pathogen, and its complex mechanisms of antibiotic resistance pose a challenge to modern medicine. This literature review explores the advancements made from 1979 to 2024 in understanding the regulatory networks of antibiotic resistance genes in Pseudomonas aeruginosa, with a particular focus on the molecular underpinnings of these resistance mechanisms. The review highlights four main pathways involved in drug resistance: reducing outer membrane permeability, enhancing active efflux systems, producing antibiotic-inactivating enzymes, and forming biofilms. These pathways are intricately regulated by a combination of genetic regulation, transcriptional regulators, two-component signal transduction, DNA methylation, and small RNA molecules. Through an in-depth analysis and synthesis of existing literature, we identify key regulatory elements mexT, ampR, and argR as potential targets for novel antimicrobial strategies. A profound understanding of the core control nodes of drug resistance offers a new perspective for therapeutic intervention, suggesting that modulating these elements could potentially reverse resistance and restore bacterial susceptibility to antibiotics. The review looks forward to future research directions, proposing the use of gene editing and systems biology to further understand resistance mechanisms and to develop effective antimicrobial strategies against Pseudomonas aeruginosa. This review is expected to provide innovative solutions to the problem of drug resistance in infectious diseases.</p>","PeriodicalId":74218,"journal":{"name":"Molecular biomedicine","volume":"5 1","pages":"62"},"PeriodicalIF":6.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11599538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142735220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}