Frontiers in bioscience (Landmark edition)最新文献

{"title":"Hypoxia-Induced <i>VGF</i> Promotes Cell Migration and Invasion in Prostate Cancer via the PI3K/Akt Axis.","authors":"Leilei Wang, Ting Zhang, Yanning Qian, Yingying Wu, Ting Li, Yongbo Zheng, Chunli Luo, Xiaohou Wu, Tingmei Chen, Liping Ou","doi":"10.31083/FBL25522","DOIUrl":"https://doi.org/10.31083/FBL25522","url":null,"abstract":"<p><strong>Background: </strong>Metastasis is a major cause of prostate cancer (PCa)-related deaths in men. Recent studies have indicated that VGF nerve growth factor inducible (VGF) affects tumor invasion and metastasis. The present study investigated whether VGF is abnormally expressed in PCa and affects PCa progression and investigated the specific regulatory mechanisms by which VGF affects PCa invasion and metastasis.</p><p><strong>Methods: </strong>The sh- hypoxia-inducible factor1 alpha (HIF-1α) plasmid was transfected into human cell lines 22Rv1 and C4-2 to create cell lines with stable low expression and overexpression of VGF. Quantitative PCR (qPCR) was performed to detect <i>VGF</i> mRNA. Western blot was performed to detect invasive migration-related proteins. Akt activator SC79 (4 μg/mL) was added. After adding docetaxel (4 nM) to cells transfected with sh-NC and sh-VGF, the capacity of the cells to migrate invasively was assessed using the Transwell and scratch assays. Nude mice were injected with cells stably transfected with sh-NC or sh-VGF and the metastasis of the cancer cells was detected by live imaging and HE staining after the injection of docetaxel (10 mg/kg).</p><p><strong>Results: </strong>Abnormal levels of VGF in PCa tissue and plasma samples were detected, and <i>VGF</i> knockdown suppressed PCa metastasis. VGF was also shown to affect the invasion and metastasis of PCa cells via PI3K/Akt signaling. <i>VGF</i> knockdown limited PCa metastasis and the inhibitory impact was higher when paired with docetaxel (<i>p</i> < 0.001). After hypoxia induction, both the mRNA and protein levels of <i>VGF</i> and HIF-1α increased, which is associated with a poor prognosis for PCa.</p><p><strong>Conclusion: </strong>By stimulating the PI3K/Akt pathway, VGF encourages the invasive metastasis of PCa. As a result, targeting <i>VGF</i> may be a potential treatment approach for metastatic PCa therapy.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"25522"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dexmedetomidine Protects the Brain: Exploring the α2AR/FAK Pathway in Post-Stroke Intestinal Barrier Repair.","authors":"Xinting Zhou, Yan Yang, Zixuan Su, Zhonghui Luo","doi":"10.31083/FBL27159","DOIUrl":"https://doi.org/10.31083/FBL27159","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Globally, ischemic stroke is a major cause of mortality and disability, posing a significant challenge in clinical practice and public health. Recent studies have reported that stroke leads to the impairment of the intestinal barrier and the migration of intestinal bacteria to multiple organs. This process exacerbates neurological damage by further impairing intestinal barrier function and leading to bacterial translocation. Dexmedetomidine (Dex), an α2-adrenoceptor (α2AR) agonist, has proven anti-cerebral ischemic effects, yet its effects in post-stroke intestinal dysfunction remain unclear. This study aimed to determine whether Dex mitigates intestinal dysfunction and brain injury following cerebral ischemia-reperfusion.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A C57BL/6J mouse model of middle cerebral artery occlusion (MCAO) was used for &lt;i&gt;in vivo&lt;/i&gt; experiments, while lipopolysaccharide (LPS)-induced Caco-2 monolayers served as an &lt;i&gt;in vitro&lt;/i&gt; model of intestinal barrier dysfunction. Neuronal apoptosis was evaluated using neuronal nuclei (NeuN) and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) double labeling. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Intestinal permeability was assessed using histological score, serum fluorescein isothiocyanate (FITC)-dextran fluorescence, and endotoxin levels. The expression levels of epithelial cadherin (E-cadherin), zonula occludens-1 (ZO-1), and occludin were analyzed by western blot and immunofluorescence. Statistical analyses included analysis of variance with Tukey's post-hoc test.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Dex treatment significantly reduced cerebral infarct volume (&lt;i&gt;p&lt;/i&gt; &lt; 0.001) and improved neurological scores compared to MCAO controls. Neuronal apoptosis was significantly inhibited (&lt;i&gt;p&lt;/i&gt; &lt; 0.01), as evidenced by reduced TUNEL-positive cells in Dex-treatment MCAO mice. TNF-α, IL-1β and IL-6 were markedly downregulated (&lt;i&gt;p&lt;/i&gt; &lt; 0.05). While MCAO increased intestinal permeability (elevated serum FITC-dextran and endotoxin levels, &lt;i&gt;p&lt;/i&gt; &lt; 0.01), Dex treatment restored barrier integrity. Dex upregulated E-cadherin expression significantly (&lt;i&gt;p&lt;/i&gt; &lt; 0.05) but did not restore the decreased levels of ZO-1 and occludin following MCAO. Dex promoted intestinal permeability repair and alleviated brain injury via the α2AR/focal adhesion kinase (FAK) pathway in MCAO mice. Similarly, Dex mitigated LPS-induced barrier dysfunction in Caco-2 monolayers by restoring FAK expression and improving intestinal barrier integrity.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Dex alleviates post-stroke intestinal barrier dysfunction and mitigates brain injury, possibly through activating the α2AR/FAK pathway. These findings underscore a potential therapeutic strategy for addressing secondary complications of ischemic stroke and improv","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"27159"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the Pathogenic Mechanism of Spinal Muscular Atrophy Through the Investigation of <i>UTS2</i>.","authors":"Xu Zhang, Liqi Yang","doi":"10.31083/FBL28242","DOIUrl":"https://doi.org/10.31083/FBL28242","url":null,"abstract":"<p><strong>Background: </strong>Spinal muscular atrophy (SMA) is a severe neuromuscular disorder caused by mutations in the survival motor neuron 1 (<i>SMN1</i>) gene, resulting in progressive motor neuron loss and muscle atrophy. The urotensin 2 (<i>UTS2</i>) gene, located on chromosome 9q34.2, plays a significant role in cellular activities such as proliferation, apoptosis, and inflammatory responses. Notably, elevated expression levels of <i>UTS2</i> have been observed in SMA patients. However, its precise contribution to disease pathogenesis remains unclear. This study aimed to investigate the effects of <i>UTS2</i>, which is overexpressed in SMA patients, in SMA cell models using a UTS2 inhibitor.</p><p><strong>Methods: </strong>We conducted genomic sequencing and bioinformatics analysis on clinical samples to identify proteins highly expressed in association with SMA. Using RNA interference technology, we suppressed <i>SMN1</i> gene expression in bone marrow mesenchymal stem cells (MSCs) to establish an <i>in vitro</i> cellular model of SMA. To assess the biological consequences of <i>SMN1</i> gene knockdown, we employed molecular biological techniques such as immunofluorescence, reverse transcription quantitative polymerase chain reaction (RT-qPCR), and western blotting. Furthermore, we treated the SMA cellular model with the urantide UTS2 receptor inhibitor and examined its effects on cell proliferation, apoptosis, and the expression of relevant proteins.</p><p><strong>Results: </strong>UTS2 was successfully identified as a highly expressed protein associated with SMA. A stable MSC model with <i>SMN1</i> gene knockdown was established. RNA interference (RNAi) technology effectively suppressed <i>SMN1</i> gene expression, leading to changes in cellular morphology and neuron-specific marker expression. Urantide intervention significantly affected both proliferation and apoptosis in the SMA cell model in a dose-dependent manner. Techniques such as the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, TUNEL fluorescence staining, and flow cytometry analysis revealed that uride decreased cell viability while increasing the proportion of apoptotic cells. Following urantide intervention, there was a notable increase in caspase-3 messenger ribonucleic acid (mRNA) levels, as well as an increase in caspase-3 protein expression, as demonstrated by immunofluorescence analysis.</p><p><strong>Conclusion: </strong>We elucidated the role of the <i>UTS2</i> gene in an SMA cell model, emphasizing its dysregulation and identifying potential therapeutic targets. Urantide, a UTS2 inhibitor, had significant biological effects on the SMA cell model, indicating that it is a promising therapeutic strategy for SMA. These findings provide valuable insights for advancing drug development and clinical treatment of SMA.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"28242"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N-acetyltransferase 10 Promotes Cervical Cancer Progression Via N4-acetylation of <i>SLC7A5</i> mRNA.","authors":"Peili Liang, Dongmei Zhou, Jinrong Liao, Wujiang Lai, Xiujie Sheng, Yifeng Wang","doi":"10.31083/FBL26756","DOIUrl":"https://doi.org/10.31083/FBL26756","url":null,"abstract":"<p><strong>Introduction: </strong>N-acetyltransferase 10 (NAT10) mediates N4-acetylcytidine (<i>ac4C</i>) mRNA modification and promotes malignant tumor progression. However, there has been limited research on its role in cervical cancer. This study aimed to decipher the role of NAT10 in cervical cancer.</p><p><strong>Methods: </strong>The prognostic value of NAT10 was explored using the cancer genome atlas (TCGA) database and immunohistochemistry of cervical cancer tissue. The biological actions of NAT10 in cervical cancer were investigated by cell proliferation, transwell, wound healing, and chicken chorioallantoic membrane assays. The therapeutic action of remodelin (a NAT10 inhibitor) was verified in a nude mouse model. Mechanistic analyses were conducted by RNA sequencing, ac4C dot blotting, acetylated RNA immunoprecipitation, quantitative PCR, and RNA stability experiments.</p><p><strong>Results: </strong>NAT10 was overexpressed in cervical carcinoma and its overexpression was associated with poor prognosis. NAT10 knockout impaired proliferative and metastatic potentials of cervical cancer cells, while its overexpression had the opposite effects. Remodelin impaired cervical cancer proliferation <i>in vivo</i> and <i>in vitro</i>. NAT10 acetylated solute carrier family 7 member 5 (<i>SLC7A5</i>) enhanced mRNA stability to regulate SLC7A5 expression.</p><p><strong>Conclusions: </strong>NAT10 exerts a critical role in cervical cancer progression via acetylating <i>SLC7A5</i> mRNA and could represent a key prognostic and therapeutic target in cervical cancer.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"26756"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Neuropeptide B/W Signaling in Modulating Intracellular Calcium in Human Skin Fibroblasts.","authors":"Shashank Pandey, Elisa Peroni, Dagmar Jarkovska, Magdalena Chottova Dvorakova, Olivier Monasson, Michal Jirasko, Tomas Chmelir, Radek Kučera","doi":"10.31083/FBL26760","DOIUrl":"https://doi.org/10.31083/FBL26760","url":null,"abstract":"<p><strong>Background: </strong>The neuropeptide B/W signalling system (NPB/W) has been identified in multiple body regions and is integral to several physiological processes, including the regulation of food intake and energy homeostasis. Recently, it has also been detected in human skin; however, its specific functions in this context remain to be thoroughly investigated. This study aims to identify the expression of neuropeptides B/W receptor 1 (NPBWR1) and neuropeptides B/W receptor 2 (NPBWR2) in human dermal fibroblasts of mesenchymal origin using genomic and proteomic techniques. We will also investigate the role of these receptors in cell proliferation and calcium signalling.</p><p><strong>Methods: </strong>The mRNAs for <i>NPBWR1</i> and <i>NPBWR2</i> were detected using quantitative PCR (qPCR) analysis and further validated by western blot and immunofluorescence analyses. Additionally, we synthesised ligands for these receptors, specifically hNPB (25-53) and hNPW (33-62), to investigate their effects on cell proliferation and intracellular calcium levels in human fibroblasts.</p><p><strong>Results: </strong>Our results demonstrated that hNPW (33-62) has anti-proliferative effect on human dermal fibroblasts and concentration of 0.1-μmol/L can significantly decrease intracellular calcium levels (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>This finding suggests a potential role for the NPB/W signalling system in pathologies associated with impaired calcium handling, such as fibrosis. Furthermore, we observed that the proliferation of human fibroblasts was not affected by hNPB (25-53). Our findings could lead to the development of new therapeutic strategies for various skin conditions and improved wound healing.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"26760"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Markers of Occult Lymph Node Metastasis in Head and Neck Squamous Cell Carcinoma (HNSCC) Patients.","authors":"Piero Giuseppe Meliante, Sofia Pizzolante, Luca Perna, Chiara Filippi, Giorgio Bandiera, Christian Barbato, Antonio Minni, Marco de Vincentiis, Edoardo Covelli","doi":"10.31083/FBL25267","DOIUrl":"https://doi.org/10.31083/FBL25267","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The accurate diagnosis of regional lymph node metastasis is critical for guiding treatment decisions in head and neck cancer patients. Despite advances in imaging techniques, detecting nodal metastasis using radiology remains challenging, leading to potential undertreatment or overtreatment. This review aims to identify molecular markers associated with occult metastasis in head and neck squamous cell carcinoma (HNSCC) patients. We divided the results by subsite for markers: lymph node analysis (microRNAs, myosin-5a (MYO5A), ring finger protein 145 (RNF145), F-box only protein 32 (FBXO32), CTONG2002744, cytokeratin 14 (CK14), eukaryotic initiation factor 4E (eIF4E), desmoglein-3 (DSG3), microsatellite D9S171, squamous cell carcinoma antigen, cytokeratin, tumor budding score, human papillomavirus-DNA (HPV-DNA), tumor infiltrating lymphocytes, sentinel lymph node analysis techniques, single fiber reflectance spectroscopy, radiological techniques), tumor tissue analysis (activin A, carcinoma-associated fibroblasts, cyclins, β-catenin, histopathology, genetic amplifications, DNA methylation, ecotropic viral integration site 1, CC-chemokine receptor 7, melanoma associated-A antigens, vascular endothelial growth factor-C (VEGF-C), panitumumab, epidermal growth factor receptor (EGFR), cornulin, total protein analysis, CD133, NANOG homeobox, neurogenic locus notch homolog protein 1 (NOTCH1), metastasis-associated protein 1, 14-3-3-zeta, E-cadherin, focal adhesion kinase, p-epithelial-mesenchymal transition (EMT), small proline rich protein 1B (SPRR1B), transcription factor NKX3-1, DNA copy number aberrations, microfibril-associated protein 5 (MFAP5), troponin C1, slow skeletal and cardiac type (TNNC1), matrix Gla protein (MGP), fibroblast growth factor binding protein 1 (FBFBP1), F-box protein 32 (FBXO32), fatty acid binding protein 5, B cell-specific Moloney murine leukemia virus integration site 1, podoplanin, p53, Bcl-2, epidermal growth factor receptor (EGFR), Ki67, cyclin D1, cox-2, semaphorin-3F, neuropilin-2, histologic features, cellular dissociation grade, prospero homeobox protein 1, radiologic features, Ki-67, poly (ADP-ribose) polymerase (PARP), Bcl-2 associated agonist of cell death (BAD), caspase-9, vascular endothelial growth factor A (VEGF-A), HPV, p16, methylation status of long interspersed element 1 (LINE-1) and Alu elements, mesenchymal-epithelial transition (MET), gene expression analyses, molecular subtypes) and blood markers (standard blood analysis indexes and ratios, circulating tumor cells, HPV-DNA, CD-31, bone marrow analysis). Several promising markers were identified, including miR-205, desmoglein 3 (DSG3), pan-cytokeratin (CK) AE1/AE3, HPV-16, activin-A, cyclin D1, E-cadherin, and neural progenitor lineage (NPL) that demonstrated effectiveness across multiple studies. Future research should focus on exploring combination scoring systems to improve diagnostic precision and optimize treatment selection in HNSCC patients.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"25267"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding Plants' Language: A Contribute to Tackling Plant Blindness.","authors":"Jorge Marques da Silva","doi":"10.31083/FBL36249","DOIUrl":"https://doi.org/10.31083/FBL36249","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"36249"},"PeriodicalIF":3.3,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress in Pediatric Asthma: Sources, Mechanisms, and Therapeutic Potential of Antioxidants.","authors":"Yanhua Han, Mingyao Zhang, Shishu Yu, Lulu Jia","doi":"10.31083/FBL22688","DOIUrl":"https://doi.org/10.31083/FBL22688","url":null,"abstract":"<p><p>Pediatric asthma is a common respiratory condition in children, characterized by a complex interplay of environmental and genetic factors. Evidence shows that the airways of stimulated asthmatic patients have increased oxidative stress, but the exact mechanisms through which this stress contributes to asthma progression are not fully understood. Oxidative stress originates from inflammatory cells in the airways, producing significant amounts of reactive oxygen species (ROS) and reactive nitrogen species (RNS). External factors such as cigarette smoke, particulate matter, and atmospheric pollutants also contribute to ROS and RNS levels. The accumulation of these reactive species disrupts the cellular redox balance, leading to heightened oxidative stress, which activates cellular signaling pathways and modulates the release of inflammatory factors, worsening asthma inflammation. Therefore, understanding the sources and impacts of oxidative stress in pediatric asthma is crucial to developing antioxidant-based treatments. This review examines the sources of oxidative stress in children with asthma, the role of oxidative stress in asthma development, and the potential of antioxidants as a therapeutic strategy for pediatric asthma.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"22688"},"PeriodicalIF":3.3,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Inflammasome: A Promising Potential Therapeutic Target for Early Brain Injury Following Subarachnoid Hemorrhage.","authors":"Xi Zhang, Chao Xu, Zi-Yuan Liu, Dong-Yuan Zhang, Bo-Hong Wang, Jing Wang, Xin-Min Ding","doi":"10.31083/FBL33454","DOIUrl":"https://doi.org/10.31083/FBL33454","url":null,"abstract":"<p><p>Subarachnoid hemorrhage (SAH), a severe cerebrovascular disorder, is principally instigated by the rupture of an aneurysm. Early brain injury (EBI), which gives rise to neuronal demise, microcirculation impairments, disruption of the blood-brain barrier, cerebral edema, and the activation of oxidative cascades, has been established as the predominant cause of mortality among patients with SAH. These pathophysiological processes hinge on the activation of inflammasomes, specifically the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)and absent in melanoma 2 (AIM2) inflammasomes. These inflammasomes assume a crucial role in downstream intracellular signaling pathways and hold particular significance within the nervous system. The activation of inflammasomes can be modulated, either by independently regulating these two entities or by influencing their engagement at specific target loci within the pathway, thereby attenuating EBI subsequent to SAH. Although certain clinical instances lend credence to this perspective, more in-depth investigations are essential to ascertain the optimal treatment regimen, encompassing dosage, timing, administration route, and frequency. Consequently, targeting the ensuing early brain injury following SAH represents a potentially efficacious therapeutic approach.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"33454"},"PeriodicalIF":3.3,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stellate Ganglionectomy Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction.","authors":"Hui Yan, Xiujun Li, Beilei Liu, Bin Wu, Changgui Chen, Liqun He, Gang Wu","doi":"10.31083/FBL26268","DOIUrl":"https://doi.org/10.31083/FBL26268","url":null,"abstract":"<p><strong>Background: </strong>Enhanced cardiac sympathetic activity contributes to chronic heart failure (CHF). Interventions targeting the stellate ganglion (SG) can reduce this activity, potentially slowing the progression of cardiovascular diseases. This study examined the effects and mechanisms of stellate ganglionectomy on myocardial hypertrophy and cardiac dysfunction caused by pressure overload.</p><p><strong>Methods: </strong>A rat model of pressure overload was created using abdominal aortic constriction. Four groups were studied: the sham surgery, abdominal aortic coarctation (AB), aortic constriction plus left stellate ganglionectomy (LSG), and aortic constriction plus right stellate ganglionectomy (RSG) groups. Cardiac function was assessed via echocardiography, and myocardial hypertrophy and fibrosis were evaluated using hematoxylin-eosin staining (H&E) and Masson staining. Serum atrial natriuretic peptides (ANP) and norepinephrine (NE) levels were measured using enzyme linked immunosorbent assay (ELISA), and the levels of the molecular markers tyrosine hydroxylase (TH) and growth-associated protein-43 (GAP43) were analyzed using Western blotting and PCR. Calcium calmodulin dependent protein kinase II (CaMKII) and phosphorylated Ryanodine Receptor 2 (p-RyR2) expression were also investigated.</p><p><strong>Results: </strong>Stellate ganglionectomy significantly reduced myocardial hypertrophy and improved cardiac function, as indicated by decreased left ventricular posterior wall thickness (LVPWD) (<i>p <</i> 0.01), left ventricular end-diastolic diameter (LVEDD) and volume (<i>p</i> < 0.001), left ventricular end-diastolic volume (LVEDV) (<i>p</i> < 0.001), increased left ventricular ejection fraction (LVEF) (<i>p</i> < 0.001) and left ventricular fractional shortening (LVFS) (<i>p</i> < 0.001). Histological analysis confirmed reduced myocardial dilation. Molecular analysis revealed decreased CaMKII/RyR2 signaling (<i>p</i> < 0.001) and lower NE levels (<i>p</i> < 0.01), suggesting reduced neurohormonal stress.</p><p><strong>Conclusions: </strong>Stellate ganglionectomy alleviates hypertrophy and cardiac dysfunction caused by pressure overload, likely through inhibition of the CaMKII/RyR2 pathway, underscoring its potential as a therapeutic approach.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"26268"},"PeriodicalIF":3.3,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}