Biomolecules最新文献

{"title":"Low Silicon Content in Leaves and Higher Deposition in Roots Is Associated with <i>Lsi</i> Genes in <i>Psathyrostachys juncea</i>: Microscopy, Gene Expression and Genotyping Study.","authors":"Svetlana Dashkevich, Maral Utebayev, Nadezhda Filippova, Oksana Kradetskaya, Irina Chilimova, Botagoz Sharipova, Gulmira Khassanova, Marzhan Kuzbakova, Satyvaldy Jatayev, Nurgul Daniyeva, Yuri Shavrukov","doi":"10.3390/biom16091351","DOIUrl":"10.3390/biom16091351","url":null,"abstract":"<p><p>Accessions of Russian wildrye, <i>Psathyrostachys juncea</i>, an important pasture fodder crop, were arranged in group A with high silicon content in leaves and group B with low silicon content. Scanning electron microscopy (SEM) and energy-dispersive X-ray spectroscopy (EDS) analyses revealed low Si accumulation in roots but higher deposition in leaves of plants from group A, whereas, in contrast, plants from group B showed significantly higher Si content in roots but lower in leaves. Three identified <i>PjLsi</i> genes encoding influx and efflux of silicon were differentially expressed, with higher levels in plants from group A, including <i>PjLsi1</i> and <i>PjLsi3</i> in leaves, and <i>PjLsi2</i> in roots, compared to those from group B. A working model was proposed based on differences in microscopy and gene expression analyses. Sanger sequencing revealed one SNP in the conservative gene <i>PjLsi1</i>, and 14 and 29 SNPs in the more polymorphic DNA sequences of <i>PjLsi2</i> and <i>PjLsi3</i>, respectively. Allele-specific qPCR (ASQ) markers were developed based on optimally identified SNPs and successfully used for genotyping of all three <i>PjLsi</i> genes in a germplasm collection comprising 72 <i>P. juncea</i> accessions. Highly significant differences were found between groups of genotypes in all three <i>PjLsi</i> genes using ASQ markers with corresponding Si content in the studied accessions, including those from groups A and B. The developed ASQ markers can be tested as candidates in marker-assisted selection for genotyping of hybrid breeding lines and for identification of the best <i>P. juncea</i> genotypes with minimal Si content in leaves of pasture fodder crop.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex, Sex Hormones and Inflammatory Burden and Cardiovascular Risk in Patients with Spondyloarthritis.","authors":"Isaac T Cheng, Huan Meng, Ho So, Lai Shan Tam","doi":"10.3390/biom16091345","DOIUrl":"10.3390/biom16091345","url":null,"abstract":"<p><p>Spondyloarthritis encompasses a spectrum of inflammatory diseases, including axial spondyloarthritis and peripheral forms such as psoriatic arthritis. Chronic inflammation is closely linked to an increased risk of cardiovascular (CV) disease in these patients. Beyond inflammatory burden, biological sex and sex hormones may modify both inflammatory pathways and CV risk. Although the mechanisms underlying sex differences in spondyloarthritis remain incompletely understood, emerging evidence suggests clinically relevant differences in disease manifestations, inflammatory activity, and CV outcomes between males and females. This review summarizes current evidence on the interplay between sex, sex hormones, inflammatory burden, and CV risk in patients with spondyloarthritis, and highlights potential implications for risk stratification and future research.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determinants of C₁₆-Ceramide Binding to p53.","authors":"Madeline S Childress, Kristen A Jeffries, Sergey A Krupenko, Natalia I Krupenko","doi":"10.3390/biom16091343","DOIUrl":"10.3390/biom16091343","url":null,"abstract":"<p><p>The tumor suppressor p53 coordinates cellular stress responses, but underlying mechanisms remain incompletely understood. We previously demonstrated that, in response to metabolic stress, C₁₆-ceramide produced by ceramide synthase 6 (CerS6) directly binds to p53, thus preventing its MDM2-mediated degradation and promoting p53 activation. Here, we investigated the structural requirements and functional consequences of ceramide binding to p53. Using a panel of p53 mutants, including naturally occurring oncogenic variants, we characterized the ceramide-binding interface of p53 and the role of amino acid substitutions within this region in metabolic stress signaling. We found that disruption of ceramide binding impaired stress-induced p53-CerS6 interaction at the endoplasmic reticulum (ER), attenuated induction of p53 target genes, and reduced cellular sensitivity to stress. Of note, certain cancer-associated p53 mutants retained ceramide binding and the ability to activate stress responses. These studies were further extended to monitoring the p53-CerS6 interaction on the ER and associated membrane aggregation using fluorescence techniques. We showed that metabolic stress-induced ER remodeling was distinct from the canonical UPR. Overall, our study defines the ceramide-binding surface within the p53 DNA-binding domain and provides novel insight into the functional role of the ceramide-p53 interaction.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating Bubbles in Decompression Sickness: Pathophysiology and Experimental Models.","authors":"Zequn Jin, Qi Zhu, Juan Zheng, Baoliang Zhu, Kun Zhang, Guoyang Huang, Xuhua Yu, Weigang Xu","doi":"10.3390/biom16091339","DOIUrl":"10.3390/biom16091339","url":null,"abstract":"<p><p>Decompression sickness (DCS) is a severe condition caused by rapid reductions in ambient pressure during diving, altitude exposure, or aerospace operations, with circulating gas bubbles serving as a central initiating event. Stable nanobubbles on active hydrophobic spots along the vascular lumen can grow under decompression-induced supersaturation, detach, and enter the circulation. Their subsequent behavior is shaped by blood flow, vessel geometry, and coagulation and may lead to thrombosis and microvascular stasis. DCS pathogenesis involves three linked interfaces: the blood-bubble interface activates coagulation and complement; the bubble-endothelium interface causes mechanical injury, endothelial dysfunction, oxidative stress, and cell death; and the endothelium-immune interface, which promotes neutrophil recruitment and NETosis, driving sterile inflammation and microthrombosis. Experimental approaches reproduce different stages of this pathogenic sequence and can be broadly distinguished according to the origin of the bubbles. Whole-animal decompression models and whole-blood decompression systems incorporate pressure reduction or gas supersaturation and can therefore generate bubbles within the experimental system. Many endothelial-cell, vessel-based, and microfluidic platforms use pre-existing or externally generated gas bubbles that are introduced directly into the experimental system. These directly introduced-bubble models do not reproduce decompression-induced bubble genesis; however, they provide precise control over bubble size, flow, vascular geometry, and cellular interactions. They are therefore valuable for dissecting post-formation processes shared by decompression-generated and directly introduced intravascular bubbles, including bubble transport, vascular retention, endothelial injury, thrombosis, and inflammation. Recognizing this distinction in bubble origin is essential for defining the translational relevance and limitations of individual experimental models.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted Regulation of Pancreatic Islet Function by Natural Products Against Type 2 Diabetes Mellitus: Advances and Prospects.","authors":"Guanrong Qiao, Oluwaniyi Isaiah Adejobi, Xuefang Li, Yaqin Yang, Xudong He, Li Li, Yue Zhou, Jiawei Li, Hao Li, Fan Zhang, Jie Yu","doi":"10.3390/biom16091338","DOIUrl":"10.3390/biom16091338","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) is a major global health challenge, with insulin resistance (IR) and islet dysfunction as its core pathophysiology. Current glucose-lowering agents, including insulin secretagogues, insulin sensitizers, DPP-IV inhibitors, SGLT-2 inhibitors, and GLP-1 receptor agonists, effectively control blood glucose and may partly improve β-cell function indirectly, but they do not directly target the functional defects of pancreatic β cells. Developing drugs that precisely modulate islet function is therefore a key direction. Natural products, with their structural diversity, established glucose-lowering activity, and derivation from medicinal plants with long clinical use, have become an important source of lead compounds for drugs targeting these mechanisms. The main pathways through which natural products act include: (1) promoting insulin secretion through direct and indirect secretagogue mechanisms (modulating ion channels, metabolic enzymes, incretin signaling); (2) preserving β-cell function and mass by maintaining the differentiated phenotype, promoting regeneration, alleviating oxidative stress, inhibiting apoptosis and pyroptosis, attenuating inflammation, and suppressing hIAPP toxic aggregation and endoplasmic reticulum stress; and (3) other pathways with incompletely elucidated mechanisms that also contribute to islet protection. This article delineates these molecular mechanisms and highlights the limited ability of current agents to directly restore and protect β-cell function. It provides a theoretical basis for developing novel drugs that integrate glycemic control with islet restoration based on natural lead compounds, and offers a framework for further mechanistic studies. In addition, it encourages the exploration of unidentified active constituents and unique pathways, while also addressing challenges such as target identification and structure-activity relationships.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue-Specific Angiogenic Responses to Exercise: Mechanisms and Research Advances.","authors":"Xingwen Zheng, Zhijian Rao, Zhitong Sun, Yibing Lu, Lifang Zheng, Yu Feng","doi":"10.3390/biom16091340","DOIUrl":"10.3390/biom16091340","url":null,"abstract":"<p><p>Exercise is a pivotal non-pharmacological intervention for enhancing overall health, with a key underlying mechanism being the induction of adaptive angiogenesis across multiple organ systems. This narrative review discusses recent advances in exercise-induced angiogenesis, with a particular focus on its tissue- and organ-specific manifestations and underlying molecular mechanisms. The available evidence indicates that exercise integrates diverse signals-including mechanical stress, metabolic shifts, and hypoxic or ischemic stress-to upregulate key angiogenic factors, such as vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2), and to activate conserved signaling pathways including hypoxia-inducible factor-1α (HIF-1α), phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), and endothelial nitric oxide synthase (eNOS), thereby driving angiogenesis. This process exhibits tissue specificity: in skeletal muscle, it primarily enhances oxygen transport and metabolic efficiency; in bone, it couples with osteogenesis to maintain structural integrity; in the brain, it supports neuroplasticity and cognitive function; in the heart, it improves myocardial perfusion via angiogenesis and collateral remodeling (arteriogenesis); and in adipose tissue, it ameliorates the metabolic microenvironment. Furthermore, the mode and intensity of exercise, along with individual differences (such as age and health status), significantly influence the magnitude of its angiogenic effects. Accordingly, this review highlights the proposed role of exercise-induced angiogenesis in a range of conditions-including cardiovascular disease, sarcopenia, osteoporosis, neurodegenerative disorders, and metabolic syndrome-and we treat these relationships as potential mechanisms that require further validation rather than established therapeutic pathways. In the future, research should aim to define optimal exercise parameters, elucidate deeper molecular mechanisms, and investigate the translational potential of these insights for personalized clinical interventions.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Novel Transcriptional Alleles in Primary Prostate Cancer Cells and Cancer Stem Cells by Bulk RNA-Seq and Single-Cell RNA-Seq Analyses.","authors":"Wen-Yang Hu, Ranli Lu, Mark Maienschein-Cline, Duoling Xu, Parivash Afradiasbagharani, Lynn A Birch, Larisa Nonn, Andre Kajdacsy-Balla, Toshi Shioda, Gail S Prins","doi":"10.3390/biom16091341","DOIUrl":"10.3390/biom16091341","url":null,"abstract":"<p><p>Genetic alterations are closely associated with prostate cancer development and progression, but the RNA-derived transcriptional allele landscape of prostate cancer and cancer stem cells (CSCs) remains poorly understood. To characterize cancer-associated transcriptional alleles, we analyzed bulk and single-cell RNA sequencing (RNA-seq) data from primary human prostate cancer cells and their matched benign epithelial cells from non-cancerous regions of the same patients. Sequencing reads were aligned to the human reference genome (hg38) using STAR, and sequence variants were annotated with ANNOVAR. Most detected transcriptional alleles were located in noncoding regions, particularly within 3' and 5' untranslated regions, with single-nucleotide variants predominating and C>T substitutions occurring most frequently. Comparison of cancer and matched benign samples identified 223 genes carrying cancer-associated transcriptional alleles consistently detected across three independent patients. Seven of these genes showed differential expression between CSC and non-CSC populations, while 19 contained non-synonymous alleles, including 11 that are predicted to have potentially damaging effects. We identified ATF6 and KDM3A as candidate genes of potential functional interest. Single-cell RNA-seq analyses revealed differences in the number and distribution of detected transcriptional alleles between culture conditions, with 2D cancer cultures detecting more total, coding, and non-synonymous alleles than CSC-enriched 3D spheroids. CSC populations also exhibited fewer detected transcriptional alleles than non-CSC populations. Our findings provide a framework for characterizing transcriptional allele heterogeneity within the prostate cancer cellular hierarchy and identify candidate CSC-associated alterations for further investigation and functional validation. Finally, the cancer-benign matched strategy used in this study provides additional molecular evidence supporting the malignant origin of the tumor-derived cancer cells.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Regulatory System in Brain Development and Death Driven by a Bioactive Peptide Linked to a Specific Isoform of Acetylcholinesterase.","authors":"Adam Mohammed Khan, María-Salud García-Ayllón, Owen Hollings, Sara Garcia-Ratés, Susan Greenfield","doi":"10.3390/biom16091336","DOIUrl":"10.3390/biom16091336","url":null,"abstract":"<p><strong>Background: </strong>Acetylcholinesterase (AChE) demonstrates non-enzymatic actions attributable to a 14mer bioactive peptide derived from its sixth exon, 'T14', a pivotal agent driving Alzheimer's disease (AD).</p><p><strong>Methods: </strong>To investigate this possible parallel between development and neurodegeneration, we tracked the expression and timeline of T14 in embryonic and neonatal rodent brain tissue in relation to the expression of its parent molecule, AChE, benchmarked against markers of neural maturation (NeuN) and neurodegenerative pathology (pTau) using sedimentation profiling, Western blotting, and qPCR.</p><p><strong>Results: </strong>We report two key findings: Firstly, while overall AChE activity, expression, and oligomeric assembly in the developing rodent cortex predominantly reflect AChE-T, endogenous T14 appear to selectively correspond with the AChE-R variant (r = 0.936, <i>p</i> = 0.0639), peaking at P7 before declining in tandem with NeuN and pTau. Secondly, application of exogenous peptide to cultured SHSY-5Y cells triggers the selective upregulation of this same variant, AChE-R (F_(3,18) = 9.320, <i>p</i> < 0.05). This effect is blocked by cotreatment with either mTORC1 inhibitor rapamycin or NBP14, an antagonist of T14.</p><p><strong>Conclusions: </strong>We conclude that in development, T14 and AChE-R are closely linked, that both are involved in a developmental mechanism most active in the embryonic brain, and that inappropriate reactivation of this mechanism in the mature brain could be the driver in the progression of AD.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.","authors":"Tadahiko Matsumoto, Akifumi Takaori-Kondo","doi":"10.3390/biom16091344","DOIUrl":"10.3390/biom16091344","url":null,"abstract":"<p><p>Telomeres (chromosome-end nucleoprotein complexes) are prone to replication fork stalling because of their G-rich repetitive sequences, G-quadruplexes, t-loops, oxidative lesions, and telomeric R-loops generated when telomeric repeat-containing RNA (TERRA) hybridizes with telomeric DNA. In this review, we will summarize how telomeres are replicated and maintained and the mechanisms by which replication stress occurs at telomeres. Subsequently, we will review the role of POT1 mutations in cancer development and pathology and discuss therapeutic strategies targeting telomere biology in cancer.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Picropodophyllotoxin Suppresses Factor Xa Activity, Platelet Aggregation, and Arterial Thrombosis.","authors":"Gyuri Han, Ga Eun Kim, Min Seo Kim, Jaehong Kim, Jong-Sup Bae","doi":"10.3390/biom16091337","DOIUrl":"10.3390/biom16091337","url":null,"abstract":"<p><p>Picropodophyllotoxin (PPT), a naturally occurring tyrosine kinase inhibitor derived from <i>Podophyllum hexandrum</i> roots, is well recognized for its anticancer potential. The present study was designed to determine whether PPT exerts antithrombotic effects and to elucidate the underlying mechanisms. A range of functional assays were employed, including coagulation time measurements, platelet aggregation tests, evaluations of factor Xa activity and production, nitric oxide (NO) level assessments, and protein expression analyses. Our results demonstrated that PPT prolonged the clotting time of human platelet-poor plasma to an extent comparable to that of rivaroxaban, a reference anticoagulant, and effectively suppressed platelet aggregation induced by ADP or the thromboxane A2 mimetic U46619. Mechanistically, PPT inhibited the phosphorylation of PLCγ2 and PKC, as well as intracellular calcium mobilization-key events in platelet activation. It also downregulated the surface expression of the adhesion molecules P-selectin and PAC-1. In endothelial cells, PPT enhanced NO production while reducing endothelin-1 secretion following stimulation with ADP or U46619. Furthermore, PPT suppressed both the enzymatic activity and the cellular production of coagulation factor Xa in endothelial cells and blocked FXa-induced platelet aggregation. In murine models of thromboembolism, PPT administration significantly accelerated thrombus resolution, reduced thrombus burden and size, and improved survival rates. Collectively, these findings establish that PPT possesses potent antithrombotic activity, operating through prolongation of clotting time, inhibition of platelet aggregation, and suppression of factor Xa function-effects comparable to those of standard anticoagulants. This multifaceted mechanism positions PPT as a promising candidate for thrombosis therapy with a potentially favorable side-effect profile.</p>","PeriodicalId":8943,"journal":{"name":"Biomolecules","volume":"16 9","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}