Metabolic brain disease最新文献

{"title":"Unraveling novel mechanisms of ATP-Binding cassette (ABC) transporter in insulin Resistance-induced amyloidogenesis.","authors":"Akhil Sharma, Ashi Mannan, Thakur Gurjeet Singh","doi":"10.1007/s11011-025-01642-6","DOIUrl":"10.1007/s11011-025-01642-6","url":null,"abstract":"<p><p>Insulin resistance (IR) impairs glucose uptake and metabolism, whereas amyloidogenesis, the formation of abnormal protein aggregation, forming insoluble fibrils called amyloids, which are linked with numerous neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD), Huntington disease's (HD), Parkinson's disease (PD) and Prion's disease. This review explores how IR promotes amyloidogenesis by disrupting cholesterol homeostasis and enhancing Amyloid beta (Aβ) production and aggregation. Specifically, we examine the role of ATP-binding cassette (ABC) transporters in cholesterol homeostasis along with their impact on insulin signaling pathways, highlights how their dysregulation can lead to IR, a significant contributor to the development of amyloidogenesis, a key factor in causing NDDs. We explore the novel molecular mechanisms linking IR and Aβ aggregation, focusing on the interplay between ABC transporters and Amyloid precursor protein (APP) processing. Furthermore, we also explore emerging evidence linking ABC transporters to oxidative stress, inflammation and mitochondrial dysfunction critical factors in the development of amyloidogenesis. Additionally, this review also discusses potential therapeutic strategies targeting ABC transporters to mitigate IR and reduce amyloid burden by various mechanisms including Insulin receptors/IRS-1 signaling, Phosphatidylinositol3kinase-Protein kinase-B (PI3K/AKT), Mitogen-activated protein kinases (MAPK), c-Jun N-terminal kinase (JNK), Glycogen synthase kinase 3 (GSK3), mammalian Target of Rapamycin (mTOR), Insulin-Degrading Enzyme (IDE), Advanced glycation end products (AGEs), Glucose transporters (GLUTs), Apolipoprotein E (ApoE), Peroxisome proliferator-activated receptors (PPARs), Adiponectin, Mitochondrial dysfunctioning, AMP-activated protein kinase (AMPK) Wingless-related integration site/beta-catenin (Wnt/β-catenin) and Sirtuin1 (SIRT1). These insights provide new possibilities for developing targeted therapies against neurodegenerative diseases associated with IR and amyloid accumulation.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"218"},"PeriodicalIF":3.2,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting NOX inhibitors in neurodegeneration: a therapeutic perspective.","authors":"Sifat Kaur, Reet Verma, Veerta Sharma, Thakur Gurjeet Singh","doi":"10.1007/s11011-025-01644-4","DOIUrl":"10.1007/s11011-025-01644-4","url":null,"abstract":"<p><p>Neurodegenerative diseases are characterized by progressive neuronal loss, cognitive decline, and motor dysfunction driven by oxidative stress and neuroinflammation. NADPH oxidases (NOX) are a major source of reactive oxygen species (ROS) in the central nervous system, contributing to oxidative damage, mitochondrial dysfunction, and neuroinflammatory responses. Overactivation of NOX enzymes, particularly NOX-1, NOX-2, and NOX-4, has been implicated in neuronal injury and disease progression. NOX inhibitors have shown promise in pre-clinical models by reducing ROS production, modulating neuroinflammatory pathways, and preserving neuronal integrity. Despite these encouraging findings, clinical research remains in early stages, with ongoing studies focused on evaluating NOX inhibitors in neurodegeneration. NOX inhibition represents a promising therapeutic strategy for neurodegeneration. However, challenges such as achieving isoform selectivity, improving drug bioavailability, and overcoming blood-brain barrier penetration must be addressed for successful clinical translation. This review provides a therapeutic perspective on NOX inhibition in neurodegenerative diseases, discussing the current state of pre-clinical and clinical research, highlighting key challenges, and proposing directions for future research aimed at optimizing NOX-targeted therapies for clinical application.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"219"},"PeriodicalIF":3.2,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of N-acetylcysteine on apoptosis and NGF-Akt/Bad pathway in the hippocampus tissue of cerebral ischemia-reperfusion in male rats.","authors":"Hamed Saniei, Roya Naderi","doi":"10.1007/s11011-025-01641-7","DOIUrl":"10.1007/s11011-025-01641-7","url":null,"abstract":"<p><p>Apoptosis is the primary pathological feature of neuronal injury caused by cerebral ischemia-reperfusion (I/R). The detailed molecular mediators are still being debated. This study aims to examine the effects of cerebral ischemia-reperfusion on apoptosis and NGF-Akt/Bad axis in rat hippocampus alone and in combination with NAC (N-Acetylcysteine). Rats were subjected to common carotid artery occlusion (CCAO) for 20 min followed by 24 h reperfusion. NAC (150 mg/kg) was given intraperitoneally (ip) one hour before ischemia and five minutes before reperfusion. TUNEL staining of hippocampus neurons revealed that the number of apoptotic neurons was elevated 24 h after reperfusion. At the molecular levels, I/R injury resulted in an increased protein expression of cleaved caspase3/procaspase3 ratio and cytochrome c level with a concomitant down-regulation of NGF, p-AKT/AKT, p-Bad/Bad and p-Trk/Trk ratio. NAC treatment significantly reduced the apoptotic damage and also reversed NGF, p-AKT/AKT, p-Bad/Bad, and p-Trk/Trk ratio in hippocampus neurons in I/R rats. In conclusion, our data showed that NGF-Akt/Bad axis may play a regulatory role in hippocampus cell death, providing a new target for a novel therapeutic strategy during transit ischemic stroke. NAC has been shown to reverse molecular alterations, suggesting its potential as an effective agent against hippocampal apoptosis following acute I/R injury.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"217"},"PeriodicalIF":3.2,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain morphological changes in type 2 diabetes patients with painful peripheral neuropathy.","authors":"Miao He, Jiaying Yang, Xueqing Liu, Jiamin Zhou, Xuewei Zhang, Jing Li, Xiali Shao, Wenhui Li, Yuzhou Guan, Weihong Zhang, Feng Feng","doi":"10.1007/s11011-025-01643-5","DOIUrl":"10.1007/s11011-025-01643-5","url":null,"abstract":"<p><p>We investigates changes in brain volume and cortical thickness in patients with type 2 diabetes mellitus (T2DM) and peripheral neuropathy (DPN), particularly those with neuropathic pain. 105 participants were divided into three groups: T2DM (n = 26), T2DM with DPN (n = 42), and healthy controls (HCs, n = 37). The DPN group was further divided into painless (n = 22) and painful (n = 20) subgroups. Participants underwent clinical neuropsychological testing, electromyography, and brain MRI scans. Voxel-based morphometry was used to analyze gray matter volume (GMV) and cortical thickness. Associations between morphological changes and clinical/neuropsychological indicators were assessed. Average cortical thickness of the three patient subgroups was significantly reduced compared to the HCs. GMV loss in the DPN_ pain group was confined to the cerebellum, right putamen/pallidum, and caudate, while GMV increased in the brainstem. Multiple regression analysis showed correlations between brain regions and factors such as cholesterol levels, neuropathic pain severity, and nerve amplitudes (P < 0.001). The volume of right lateral geniculate nucleus volume was linked to the DN4 score (r = 0.593, P = 0.015) and onset age (r = -0.541, P = 0.031). Specific brain regions and the cortices are more vulnerable to the effects of neuropathic pain and peripheral nerve damage.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"216"},"PeriodicalIF":3.2,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144192019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota and serum metabolomics unveil the role of Phellinus ribis polysaccharides in improving Alzheimer's disease symptoms in senescence-accelerated mice.","authors":"Zhiyuan Zhang, Shuai Wang, Rong Rong, Guoying Zhang, Zheng Li, Yuanyuan Li, Rongxiang Wang, Yuhong Liu, Kejian Li","doi":"10.1007/s11011-025-01632-8","DOIUrl":"10.1007/s11011-025-01632-8","url":null,"abstract":"<p><p>Alzheimer's disease (AD), a complex neurodegenerative disorder with limited therapeutic options, urgently requires innovative strategies targeting its underlying mechanisms. Phellinus ribis polysaccharides (PRG), a bioactive compound with proven neuroprotective and microbiota-modulating effects, hold promise for addressing AD pathology through gut-brain axis regulation. This study aims to investigate the effects of PRG on the gut microbiota composition and serum metabolomic profile of a senescence-accelerated mouse model (SAMP8) and to reveal its potential mechanisms in alleviating symptoms of AD. The gut microbiota composition of SAMP8 mice treated with PRG was analyzed using 16S rRNA gene sequencing. Non-targeted metabolomics, based on ultra-performance liquid chromatography quadrupole/electrostatic field orbitrap high-resolution mass spectrometry, was employed to analyze changes in metabolites in the serum samples. Spearman correlation analysis was further used to explore the association between gut microbiota and serum metabolites. PRG significantly improved gut dysbiosis in SAMP8 mice by increasing the abundance of beneficial bacterial genera, reducing pathogenic bacteria levels, and restoring the dominance of advantageous bacterial phyla. Serum metabolomics analysis revealed that PRG intervention led to significant changes in AD-related metabolites, including phenylalanine and oxidative stress markers. Combined analysis indicated a correlation between changes in gut microbiota and serum metabolites. PRG can alleviate AD symptoms in senescence-accelerated mice by regulating gut microbiota and serum metabolites, providing scientific evidence for PRG as a potential therapeutic agent for AD. This study explores the role of gut microbiota and serum metabolites under PRG intervention in neurodegenerative diseases.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"215"},"PeriodicalIF":3.2,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quinoa extract restored behavioral damage and neurotoxicity induced by a Parkinson's disease-like model in Drosophila melanogaster.","authors":"Magna Sotelo Barrientos, Marcia Rósula Poetini, Eliana Jardim Fernandes, Luana Barreto Meichtry, Elize Aparecida Santos Musachio, Stífani Machado Araujo, Sirlei Patricia Souza, Kétnne Hanna Poleto Pinto, Murilo Ricardo Sigal Carriço, Rafael Roehrs, Marina Prigol, Gustavo Petri Guerra","doi":"10.1007/s11011-025-01640-8","DOIUrl":"10.1007/s11011-025-01640-8","url":null,"abstract":"","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"214"},"PeriodicalIF":3.2,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unlocking the neuroprotective potential of peptide nucleic acids 5 (PNA5) in neurological diseases: molecular mechanisms to therapeutic approaches.","authors":"Pratyush Porel, Garry Hunjan, Navpreet Kaur, Vipul Sharma, Manpreet Kaur, Yukti Mittal, Ramandeep Kaur, Khadga Raj Aran","doi":"10.1007/s11011-025-01629-3","DOIUrl":"10.1007/s11011-025-01629-3","url":null,"abstract":"<p><p>Peptide nucleic acids (PNAs) are synthetic nucleic acid analogues offering distinct structural and functional advantages over conventional RNA and DNA, positioning them as powerful molecules in molecular biology. Recently, PNAs have gained significant attention for their potential in the prevention and management of neurological diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), stroke, traumatic brain injury (TBI), spinal cord injury (SCI), depression, and anxiety. PNA5, a specific PNA variant, is highly expressed in neocortical association regions, particularly in primates, and plays a critical role in high-level cognitive functions such as reasoning, decision-making, and problem-solving. It can form stable, sequence-specific hybridizations with nucleic acids, resist nuclease degradation, and efficiently cross cellular membranes, making them ideal candidates for targeting disease-related genes in the brain. PNA5 has shown neuroprotective properties by improving cognitive function, reducing neuroinflammation, and preserving the integrity of the blood-brain barrier (BBB). Additionally, it supports critical processes such as neural migration, axon guidance, and synaptogenesis, which are vital for maintaining proper brain function. This review explores the mechanisms by which PNAs, particularly PNA5, exert therapeutic effects in neurological disorders. It highlights their role in gene modulation, protein regulation, and potential strategies for enhancing PNA delivery to the central nervous system (CNS) and its related disorders.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"213"},"PeriodicalIF":3.2,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Acyl-CoA synthetase long-chain family member 4: a potential approach for the treatment of cerebral ischemia/reperfusion injury.","authors":"Nikita Patil, Lokesh Kumar Bhatt","doi":"10.1007/s11011-025-01638-2","DOIUrl":"10.1007/s11011-025-01638-2","url":null,"abstract":"<p><p>Cerebral ischemia/reperfusion injury causes high rates of morbidity and death. Recent studies have shown that ferroptosis, a type of controlled cell death brought on by lipid peroxidation, worsens cerebral ischemia/reperfusion injury. Acyl-CoA synthetase long-chain family member 4 (ACSL4) has emerged as a crucial enzyme in lipid metabolism and ferroptosis in the context of ischemia/reperfusion injury, influencing neuronal cell death. Increased vulnerability to ferroptosis and worsening ischemia/reperfusion injury outcomes are linked to elevated ACSL4 levels. Comprehending the molecular processes underlying ACSL4-mediated ferroptosis may result in novel approaches to treating cerebral ischemia/reperfusion injury. The present review discusses ACSL4 as a potential target for treating cerebral ischemia/reperfusion injury, focusing on ACSL4-mediated ferroptosis and signal transduction.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"212"},"PeriodicalIF":3.2,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-134-5p/BDNF/TrkB/CREB signaling pathway involved in the depression-like behaviors in mice following exposure to benzo[a]pyrene.","authors":"Tingyi Zhao, Huan Li, Yunge Jia, Na Xia, Xin Li, Hongmei Zhang","doi":"10.1007/s11011-025-01637-3","DOIUrl":"10.1007/s11011-025-01637-3","url":null,"abstract":"<p><p>Benzo[a]pyrene (B[a]P) is known to cause depression-like symptoms in mice, however, the mechanisms are still unclear. The present study aimed to establish a mouse model of depression-like behavior induced by B[a]P and to elucidate the possible underlying mechanisms. Forty robust male ICR mice were randomly categorized into 4 groups and received intraperitoneal injections (i.p.) of peanut oil or B[a]P at doses of 0.5, 2, or 10 mg/kg, 30 times over a period of 60 days. Behavioral assessments were conducted to evaluate depression-like symptoms, identify neuronal structural alterations and cellular apoptosis, and measure the protein levels of brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), phosphorylated TrkB (p-TrkB), cAMP-response element binding protein (CREB) and phosphorylated CREB (p-CREB) in the cerebral cortex. To further explore the regulatory role of miRNA, small RNA sequencing was performed in HT22 cells treated with B[a]P at concentrations of 0.2, 2, and 20 µM, which revealed the dysregulated miRNA expression profiles. The interaction between miR-134-5p and BDNF mRNA was examined, along with its inhibitory effects in both in vivo and in vitro contexts. Findings indicated that B[a]P exposure significantly induced depression-like behavior and neuronal damage in mice in a dose-dependent manner, in contrast to the controls, and was associated with a reduction in BDNF/TrkB/CREB signaling pathway proteins in the cerebral cortex. As compared to the respective controls, B[a]P exposure notably triggered an irregular miRNA expression profile (encompassing miR-10b-5p, miR-124-3p, miR-134-5p, and miR-155-5p) in both the cerebral cortex of mice and HT22 cells. Owing to its uniform alterations in expression profiles in vivo and in vitro, miR-134-5p was chosen as the target miRNA for follow-up mechanistic research employing a miR-134-5p inhibitor (at concentrations of 100 nM) in HT22 cells. Following a 48-hour in vitro treatment with B[a]P (20 µM), there was a notable reduction in proteins linked to the BDNF/TrkB/CREB signaling pathway, in contrast to DMSO controls. This decrease was markedly ameliorated in HT22 cells that had been transfected with the miR-134-5p inhibitor. The research uncovered the pivotal function of the BDNF/TrkB/CREB signaling pathway in B[a]P-induced depressive-like behavior in vivo, and showed a regulatory role of miR-134-5p in this pathway. These findings suggest a potential intervention target against the depression-like behaviors resulting from B[a]P exposure.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"210"},"PeriodicalIF":3.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective potential of carvacrol: restoration of oxidative balance and mitigation of brain injury markers in isoproterenol-induced rats.","authors":"Betül Bağcı, Şeyma Aydın, Elif Dalkılınç, Selim Çomaklı, Sefa Küçükler, Selçuk Özdemir","doi":"10.1007/s11011-025-01634-6","DOIUrl":"10.1007/s11011-025-01634-6","url":null,"abstract":"<p><p>This research investigated the protective properties of Carvacrol (CVC) against Isoproterenol (ISO)-induced oxidative stress, neuroinflammation, and mitochondrial dysfunction in rats. The findings showed that CVC treatment did not significantly modify baseline oxidative stress levels in healthy rats but successfully alleviated ISO-induced oxidative damage by augmenting antioxidant enzyme activity and diminishing lipid peroxidation, as demonstrated by a reduction in MDA levels. These findings indicate that CVC can reinstate antioxidant capability and reduce oxidative damage. Concerning neuroinflammation, ISO therapy markedly increased the expression of pro-inflammatory markers, including TNF-α, IL-1β, c-Fos, BDNF, Nfl, and GFP, signifying a robust inflammatory and damage response. The injection of CVC following ISO exposure markedly decreased the expression of these markers, suggesting that CVC may exert a neuroprotective effect by regulating the inflammatory response and mitigating neuronal and glial damage. CVC demonstrated a notable protective effect on mitochondrial integrity, evidenced by the decreased mRNA expression of mitochondrial damage markers, including NSE, s100B, CALP1, and CALM1 in the CVC-treated groups, showing that CVC mitigates mitochondrial dysfunction. The analysis revealed no significant alterations in the expression levels of Aβ40, pTau181, and tTau across all groups, indicating that these biomarkers were not substantially influenced by CVC treatment under the study's conditions. However, β-amyloid accumulation varied significantly between groups, highlighting the need for further research to explore CVC's potential implications in amyloid-related diseases. These findings endorse CVC's neuroprotective efficacy and therapeutic potential in neurological disorders associated with oxidative stress, inflammation, and mitochondrial impairment.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 5","pages":"211"},"PeriodicalIF":3.2,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}