Inflammation and regeneration最新文献

{"title":"Advancement of humanized mice and leading applications in immunological disease models.","authors":"Satoru Munakata, Yuki Imura, Sota Fujimori, Ryota Sato, Piruzyan Mariam, Yuzo Koda","doi":"10.1186/s41232-026-00427-3","DOIUrl":"10.1186/s41232-026-00427-3","url":null,"abstract":"<p><p>Disease models are used to evaluate drug candidates, and compounds that are highly effective in vivo models have traditionally been prioritized for development. While conventional 'gold standard' animal models have been central to autoimmune drug discovery, there is increasing recognition that addressing unmet medical needs requires models capable of capturing patient pathophysiology beyond the scope of these classical systems. Accordingly, models that reflect human disease mechanisms not reproducible in conventional animals are becoming increasingly important. Humanized mice are immunodeficient mice transplanted with human immune cells, hepatocytes, thymic tissue, and other components to create a human-like biological environment that cannot be replicated in wild-type mice. Research on humanized mice has advanced through efforts to reconstitute a diverse human immune system in mice, together with accumulating knowledge of patient-specific factors such as autoantibodies and autoreactive T cells. Additionally, single-cell analyses and human tissue studies are underway to recreate the human-specific disease phenomena in humanized mice. In this review, immune-system-humanized mice are used to provide a comprehensive overview of recent advances in immune-system-humanized mouse technologies, their applications to immune-related disease models, and their current utilization in drug discovery research.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177393","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":"Generation of therapeutic T cells from human induced pluripotent stem cells.","authors":"Bo Wang, Shin Kaneko","doi":"10.1186/s41232-026-00425-5","DOIUrl":"10.1186/s41232-026-00425-5","url":null,"abstract":"<p><p>T cell exhaustion remains a critical barrier in treating chronic infections and cancer. To overcome this, our laboratory has established a platform for generating \"rejuvenated\" T cells from induced pluripotent stem cells (iPSCs). This review outlines our research trajectory, transitioning from the foundational autologous \"T-iPSC\" concept to scalable, \"off-the-shelf\" allogeneic strategies. We detail the establishment of clinical-grade, xeno-free manufacturing protocols and the integration of advanced gene editing-including functional enhancement through intracellular signaling modulation, immune rejection-related gene editing to minimize immunogenicity, and optimization of synthetic receptor architectures to mitigate the risk of Graft-versus-Host Disease (GvHD) while enhancing targeting efficiency. Furthermore, we describe our activity on generating regulatory T cells from iPSC for managing autoimmune disorders and GvHD. Finally, we discuss the remaining challenges and the future roadmap for translating these therapeutic T cells into clinical practice.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13227635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059197","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":"Correction: Th9 cells at the intersection of IBD and colorectal cancer: a context-dependent factor in carcinogenesis.","authors":"Niloufar Afrough, Amin Soltani, Maryam Khosravi, Negin Yadolahi, Ali Khodadadi, Mojtaba Shohan","doi":"10.1186/s41232-026-00426-4","DOIUrl":"10.1186/s41232-026-00426-4","url":null,"abstract":"","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"46 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148044476","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":"PAFAH2 deficiency drives sepsis-induced vascular leakage by promoting ECHS1-mediated suppression of protein crotonylation and mitochondrial dysfunction.","authors":"Ruibo Yang, Yuxi Zhang, Yinyu Wu, Weichao Li, Yue Zhang, Daiqin Bao, Xiaoli Ran, Jun Zhang, Yunqin Ren, Han She, Deyu Zuo, Yaling Wang, Yi Hu, Qingxiang Mao","doi":"10.1186/s41232-026-00424-6","DOIUrl":"10.1186/s41232-026-00424-6","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. The vascular endothelial cells (VECs) play a pivotal role in the progression of sepsis-induced vascular leakage. While therapeutic strategies targeting pathogen elimination and inflammation exist, direct interventions on the endothelial barrier are limited. The mechanisms of endothelial damage related to mitochondrial dysfunction during sepsis require further elucidation.</p><p><strong>Methods: </strong>The study utilized a cecal ligation and puncture (CLP) rat model of sepsis and lipopolysaccharide (LPS)-stimulated VECs to investigate vascular leakage mechanisms. These models were utilized to investigate the changes in vascular permeability, mitochondrial function and protein crotonylation in VECs, aiming to identify potential therapeutic targets for sepsis.</p><p><strong>Results: </strong>In septic rats, significant lung injury and increased vascular leakage were observed, linked to mitochondrial dysfunction and decreased survival rates. A marked downregulation of Platelet Activating Factor Acetylhydrolase 2 (PAFAH2) in VECs was identified post-sepsis, causing an upregulation of Enoyl-CoA Hydratase, Short Chain 1 (ECHS1), which inhibited crotonylation and compromised mitochondrial function, leading to increased apoptosis of VECs. Restoration experiments showed that modulating PAFAH2 and ECHS1 levels could mitigate these adverse effects. PAFAH2 overexpression alleviated sepsis-induced vascular leakage by downregulating ECHS1 and enhancing crotonylation.</p><p><strong>Conclusions: </strong>The study identifies the PAFAH2-ECHS1 pathway as a critical axis in sepsis-induced vascular leakage, influencing mitochondrial function and crotonylation, which leads to endothelial apoptosis. These insights could guide the development of new therapies targeting the endothelial barrier for treating sepsis.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13227733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147936644","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":"Safety and efficacy profile of S-005151 (Redasemtide), in patients with chronic liver diseases: phase 2 trial.","authors":"Atsunori Tsuchiya, Yusuke Watanabe, Naruhiro Kimura, Hiroyuki Abe, Toru Setsu, Takeshi Yokoo, Hiroteru Kamimura, Akira Sakamaki, Hiroaki Saito, Masaki Tominaga, Tatsuhiko Sato, Nobutaka Kitamura, Takahiro Tanaka, Yoshitomi Kanemitsu, Masahiro Ishizawa, Haruna Miyazawa, Mototsugu Tanaka, Hiroyuki Ishikawa, Kenichi Harada, Yoshihiko Tomita, Katsuto Tamai, Shuji Terai","doi":"10.1186/s41232-026-00421-9","DOIUrl":"10.1186/s41232-026-00421-9","url":null,"abstract":"<p><strong>Background and aims: </strong>Cirrhosis is a disease of impaired liver function and fibrosis caused by long-term liver damage. However, to date, no drugs have been approved to improve liver fibrosis. We report the results of a phase 2 study of S-005151 (generic name: Redasemtide), a partial peptide of High-Mobility Group Box 1 (HMGB1), in patients with chronic liver disease.</p><p><strong>Approach and results: </strong>This single-center, non-randomized, single-arm, open-label study was performed in Japan in patients with chronic liver disease (cohort A: 5 patients, cohort B: 5 patients) caused by HCV, HBV, MASH, or alcohol, with MR elastography of ≥ 4 kPa and Child-Pugh score up to 7 points. The primary endpoint was safety; secondary endpoints were efficacy against liver injury, function, and fibrosis. One adverse event (dysphonia) was observed in cohort A and one (fever) in cohort B, both of which were mild drug-related adverse events. S-005151 was well-tolerated. Regarding efficacy, there was a trend toward improvement post-treatment, with a decrease in transaminase and improvement in tissue inflammation scores in some cases; however, there was no significant improvement in hepatic dysfunction. Regarding liver fibrosis, there was a rapid and stable decrease in serum type IV collagen 7S levels, improvement in MR elastography findings, and an increase in platelet counts in some cases; 5 of 10 patients showed a trend toward improvement in liver fibrosis.</p><p><strong>Conclusions: </strong>S-005151 is well-tolerated in patients with chronic liver disease and may have therapeutic effects, in reducing liver damage and improving liver fibrosis.</p><p><strong>Trial registration: </strong>jRCT, jRCT 2031200232, Registered 4 December 2020 ( https://jrct.mhlw.go.jp/latest-detail/jRCT2031200232 ).</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13181892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147864906","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":"Th9 cells at the intersection of IBD and colorectal cancer: a context-dependent factor in carcinogenesis.","authors":"Niloufar Afrough, Amin Soltani, Maryam Khosravi, Negin Yadolahi, Ali Khodadadi, Mojtaba Shohan","doi":"10.1186/s41232-026-00423-7","DOIUrl":"10.1186/s41232-026-00423-7","url":null,"abstract":"<p><p>The differentiation of naïve T cells into the Th9 phenotype is driven by the synergistic effects of IL-4 and TGF-β, leading to the secretion of their hallmark cytokine, interleukin-9 (IL-9). Known for their critical roles in mucosal immunopathology, Th9 cells are particularly prominent in the gastrointestinal tract, where they contribute to autoimmunity, inflammation, and tissue damage. Recent studies have highlighted the paradoxical role of Th9 cells in colorectal carcinogenesis, revealing that their function is highly context-dependent. In the chronically inflamed microenvironment of inflammatory bowel disease (IBD), Th9 cells exhibit pro-tumorigenic functions. Th9 cells drive the transition to colitis-associated cancer (CAC) by impairing intestinal barrier integrity and promoting epithelial cell survival through PU.1/IL-6/STAT3 signaling and direct oncogene upregulation. Conversely, in sporadic colorectal cancer (CRC), Th9-derived IL-9 exerts anti-tumorigenic effects by enhancing immune surveillance, specifically through the recruitment and activation of mast cells and CD8 + cytotoxic T lymphocytes. Given the complex and often contradictory reports in the literature, this review provides an in-depth analysis of the distinct molecular mechanisms by which Th9 cells shape the tumor microenvironment. By explicitly distinguishing between inflammation-driven carcinogenesis (CAC) and sporadic CRC, this article aims to reconcile current literature and discover emerging therapeutic strategies, such as targeted metabolic reprogramming, to selectively suppress pathogenic Th9 cells without compromising systemic anti-tumor immunity.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847810","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":"Tissue-resident memory T cells in organ transplantation: implications for immune homeostasis and graft outcomes.","authors":"Xinqiang Li, Ruidong Ding, Jinzhen Cai","doi":"10.1186/s41232-026-00422-8","DOIUrl":"10.1186/s41232-026-00422-8","url":null,"abstract":"<p><p>Tissue-resident memory T cells (TRMs) are a non-circulating subset of memory T cells that reside long-term in peripheral tissues. Once considered passive sentinels, TRMs are now recognized as active regulators of transplant immunity. This review summarizes their phenotypic and functional characteristics across key transplanted organs, including kidney, liver, lung, intestine, skin, and heart. Depending on their activation state and microenvironment, TRMs can promote rejection and modulate local immune balance. Advances in single-cell and spatial profiling have revealed TRM heterogeneity, donor-recipient dynamics, and distinct transcriptional programs. We also highlight therapeutic targets such as NKG2D, IL-15, RORγt, and PD-1, and discuss their potential as biomarkers and immunomodulatory tools. Understanding TRMs as both drivers and regulators of alloimmunity offers new strategies for improving transplant outcomes.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13188801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147825020","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":"Senescence of T cells and organ aging.","authors":"Masaki Ohyagi, Minako Ito, Akihiko Yoshimura","doi":"10.1186/s41232-026-00419-3","DOIUrl":"10.1186/s41232-026-00419-3","url":null,"abstract":"<p><p>Senescence of T cells is strongly linked to organismal aging through two interconnected processes: chronic low-grade inflammation and reduced immune surveillance of senescent cells. T cells are particularly vulnerable to thymic involution, hematopoietic stem cell aging, repeated homeostatic proliferation, chronic antigenic stimulation, and metabolic and mitochondrial dysfunction. As a result, aged T cells may lose their capacity to combat infection and eliminate senescent cells, while also contributing to inflammaging through the production of inflammatory cytokines. Recent preclinical studies in murine models have demonstrated that modulation of T-cell immunosenescence can ameliorate age-related diseases. These approaches include PD-1/PD-L1 blockade, senolytic chimeric antigen receptor T (CAR-T) cells, and CXCL4/platelet factor 4 (PF4). In addition, early-stage human clinical studies of caloric restriction, low-dose mTOR inhibition, thymic regeneration, and mesenchymal stromal/stem cell (MSC) therapy suggest that interventions targeting immunosenescence may provide health benefits. Moreover, in murine models of Alzheimer's disease, T cells infiltrating the brain may exert either disease-promoting or protective effects depending on the disease stage, highlighting an important point of intersection between T-cell-mediated immunosenescence and brain aging. This review summarizes the basic concepts of immunosenescence, the molecular basis of immune surveillance of senescent cells, age-associated T-cell subsets, their links to brain aging, and interventional strategies aimed at clinical translation, with particular emphasis on T-cell biology and the transcriptional regulatory network driven by NR4a.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"46 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793097","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":"Ability to form Sox17-induced hematopoietic cell clusters varies among distinct hematopoietic sites during development.","authors":"Ayumi Itabashi, Yuki Yokoi, Kiyoka Saito, Ryota Tsukahara, Gerel Melig, Koya Azuma, Naoki Iizuka, Tetsuya Taga, Ikuo Nobuhisa","doi":"10.1186/s41232-026-00420-w","DOIUrl":"10.1186/s41232-026-00420-w","url":null,"abstract":"<p><strong>Background: </strong>Definitive hematopoietic stem cells (HSCs) emerge within intra-aortic hematopoietic cell clusters (IAHCs) located in the dorsal aorta of the aorta-gonad-mesonephros (AGM) region during midgestation in the mouse embryo. Thereafter, HSCs migrate to the fetal liver (FL) and finally settle in the bone marrow (BM). We previously showed that the transcription factor Sox17 is expressed in IAHCs. Overexpression of the Sox17 gene in IAHC cells induces the formation of cell clusters in vitro that resemble IAHCs and retain hematopoietic potential. In addition, a previous report showed that Sox17-transduced hematopoietic stem/progenitor cells (HSPCs) in the BM maintained multipotency. However, whether the ability to form such cell clusters differs among hematopoietic sites has not been fully examined.</p><p><strong>Methods: </strong>We examined whether viral overexpression of the Sox17 gene in HSPCs derived from the AGM region, the FL, and the BM leads to the formation of cell clusters. To identify the candidate genes involved in cluster formation, we performed RNA sequencing (RNA-seq) analysis on Sox17-ERT-transduced cells from the AGM region and the BM cultured with or without tamoxifen. We further analyzed the ability of one candidate gene, the Procr gene, to support cluster formation and in vitro hematopoietic activity.</p><p><strong>Results: </strong>A large number of multilineage colonies were observed in Sox17-ERT-transduced tamoxifen-treated cells in all tissues examined. However, BM cells generated significantly fewer clusters than embryonic tissues under identical experimental conditions. RNA-seq analysis revealed several genes that were highly expressed in Sox17-ERT-transduced tamoxifen-treated cells from the AGM region. The Procr gene, one of these genes, was expressed in IAHCs and was found to contribute to cluster formation and to be associated with the maintenance of in vitro hematopoietic activity in Sox17-transduced cells of the AGM region.</p><p><strong>Conclusions: </strong>Our results revealed that the efficiency of cluster formation varies depending on the developmental origin of hematopoietic cells, suggesting that cluster formation and colony-forming activity can be partially dissociated during the transition from fetal to adult hematopoiesis. Moreover, the Procr gene appears to contribute to cluster formation and to be associated with enhanced in vitro hematopoietic activity in midgestation mouse embryos.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":"46 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13104338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793126","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":"Reengineering statin therapy to protect skeletal muscle: nanocarrier strategies for mitigating mitochondrial dysfunction and myotoxicity.","authors":"Obaydah Abd Alkader Alabrahim, Nageh K Allam","doi":"10.1186/s41232-026-00413-9","DOIUrl":"10.1186/s41232-026-00413-9","url":null,"abstract":"<p><p>Statins remain the cornerstone of atherosclerotic cardiovascular disease prevention; however, their long-term clinical utility is frequently limited by skeletal muscle toxicity, ranging from mild myalgia to severe myopathy. Growing evidence implicates mitochondrial dysfunction, oxidative stress, and impaired muscle energy homeostasis as central drivers of statin-induced muscle injury, with important consequences for patient adherence and treatment durability. Emerging nanocarrier-based drug delivery strategies provide an opportunity to address these limitations by reprogramming statin biodistribution, intracellular exposure, and release kinetics in a biologically informed manner. This review critically examines preclinical and early clinical studies of nanoformulated statins, including solid lipid nanoparticles, polymeric and hyaluronic acid-based carriers, nanocrystals, and porous microsponges, across widely prescribed agents such as simvastatin, atorvastatin, and pitavastatin. Across multiple animal models, nanocarrier-mediated delivery consistently enhances hepatic targeting while attenuating systemic peak exposure, leading to marked reductions in biochemical, histopathological, and functional indicators of skeletal muscle injury relative to conventional formulations. Co-encapsulation strategies incorporating mitochondrial-supportive agents, such as coenzyme Q10 or selenium, further amplify muscle protection while enabling dose reduction. Mechanistically, these protective effects are associated with preservation of mitochondrial respiratory capacity, suppression of reactive oxygen species generation, and attenuation of pro-inflammatory signaling within muscle tissue, pathways directly implicated in muscle degeneration and impaired repair. By integrating molecular mechanisms with translational considerations, this review positions nanocarrier-enabled statin delivery as a promising strategy to decouple lipid-lowering efficacy from muscle toxicity, with broader implications for safeguarding skeletal muscle health and function during chronic pharmacotherapy.</p>","PeriodicalId":94041,"journal":{"name":"Inflammation and regeneration","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13101264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147731125","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}