Biomedicines最新文献

{"title":"Metabolism and Immune Suppressive Response in Liver Cancer.","authors":"Patrizio Caini, Vinicio Carloni","doi":"10.3390/biomedicines13061461","DOIUrl":"10.3390/biomedicines13061461","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) constitutes more than 90% of the primary tumor of the liver. Metabolic reprogramming is decisive in promoting HCC development. The new metabolic program drives the surrounding immune cells to an immune suppressive commitment, enabling tumor survival. The enhanced metabolic activity of cancer cells leads to competition for essential nutrients, depriving non-malignant cells of critical resources. Simultaneously, the accumulation of metabolic byproducts within the tumor microenvironment (TME) selectively favors innate immune responses while impairing adaptive immunity. Recent advances in cancer immunotherapy underscore the importance of targeting both immune cell function and metabolic pathways. In this context, reprogramming the metabolism of effector and regulatory immune cells represents a promising therapeutic avenue. This review focuses on a relatively underexplored aspect of liver cancer immunology, the immunosuppressive role of tumor-associated macrophages (TAMs) and regulatory T cells (Tregs) driven by metabolic alterations and how these mechanisms contribute to the suppression of effective anti-tumor immune responses.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reshaping Dyslipidaemia Treatment with Bempedoic Acid-A Narrative Review.","authors":"Dominik Strikic, Zvonimir Begic, Ivana Radman, Fran Zlopasa, Jana Mateljic, Ivica Zec, Marina Titlic, Ana Marija Sliskovic, Ivan Pecin, Zeljko Reiner, Iveta Mercep","doi":"10.3390/biomedicines13061460","DOIUrl":"10.3390/biomedicines13061460","url":null,"abstract":"<p><p>Dyslipidaemia is one of the main causes of atherosclerotic cardiovascular disease (ASCVD) worldwide. Although statins remain the cornerstone of lipid-lowering therapy, many patients do not achieve optimal target levels of low-density lipoprotein cholesterol (LDL-C) due to intolerance or inadequate response. Bempedoic acid, an oral ATP citrate lyase inhibitor, provides a liver-specific mechanism that lowers LDL-C levels while minimising muscle-related side effects. Recent clinical trials, including the CLEAR Outcomes Study, have shown that bempedoic acid was able to reduce LDL-C by approximately 29 mg/dL and major adverse cardiovascular events (MACEs) by 13% in patients intolerant to statins. Combination therapy with ezetimibe further enhances this effect. However, adverse effects such as increased uric acid and gout have been reported, requiring careful patient selection and continuous monitoring. This review provides a comparative synthesis of the latest evidence on bempedoic acid, including its pharmacological profile, its efficacy in different patient groups, and its place within current treatment strategies for dyslipidaemia. It also identifies research gaps and directions for future studies.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12191183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Overview of Glutaminyl Cyclase as a Promising Drug Target for Alzheimer's Disease.","authors":"Rasajna Madhusudhana, Emily Boyle, Yana Cen","doi":"10.3390/biomedicines13061467","DOIUrl":"10.3390/biomedicines13061467","url":null,"abstract":"<p><p>Alzheimer's disease (AD) has become an increasingly pressing concern for the aging population. Current AD treatments mainly focus on cognitive and neuropsychiatric symptoms-with few FDA-approved treatments targeting disease progression itself. The amyloid cascade hypothesis describes the formation and accumulation of β-amyloid (Aβ) oligomers and plaques as a primary event in AD pathogenesis. This hypothesis has served as the foundation of disease-modifying treatment development over the last decade. Recently, glutaminyl cyclase (QC) has been identified as a potential drug target in the amyloid cascade. QC catalyzes the cyclization of Aβ to form pyroglutamated Aβ (pEAβ). pEAβ acts as the seed for the formation of Aβ plaques, thus preventing the formation of pEAβ via QC inhibition, and offers a promising therapeutic strategy against AD. Here, we offer an overview of the pathway QCI research has followed-from the initial testing of imidazole-based inhibitor scaffolds to QCI structural optimization via pharmacophore identification, Varoglutamstat entering clinical trials, and further avenues of bettering specificity and potency for future QCI development.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D Attenuates Hepatic Sinusoidal Capillarization in Type 2 Diabetes Mellitus- Metabolic Dysfunction-Associated Fatty Liver Disease via Dual Autophagy Activation and Pyroptosis Suppression in Liver Sinusoidal Endothelial Cells.","authors":"Panpan Jiang, Yang Liu, Juxiang Liu, Jinxing Quan","doi":"10.3390/biomedicines13061459","DOIUrl":"10.3390/biomedicines13061459","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Metabolic dysfunction-associated fatty liver disease (MAFLD) is closely associated with type 2 diabetes mellitus (T2DM), where T2DM serves as a crucial driving factor for MAFLD progression. While vitamin D (VD) demonstrates protective effects against MAFLD, the underlying mechanisms through which it influences MAFLD-related liver sinusoidal endothelial cell (LSEC) capillarization remain to be elucidated. This study aimed to explore how vitamin D ameliorates LSEC capillarization in T2DM-associated MAFLD. <b>Methods:</b> Culture human liver sinusoidal endothelial cells (HLSECs) according to the established protocol. After 1,25(OH)₂D₃ intervention in high glucose (HG)-induced HLSECs, determine the changes in liver sinusoidal capillarization-related proteins (LN, PLVAP), autophagy and pyroptosis levels. Observe the changes in cell lipid accumulation and fenestration structures. After adding Bafilomycin A1, MCC950, compound C and rapamycin to HLSECs, explore the therapeutic mechanism of 1,25(OH)₂D₃. After supplementing VD to MAFLD model mice, further verify the therapeutic mechanism of VD on MAFLD. <b>Results:</b> HG can induce the capillarization and lipid accumulation of HLSEC, increase the level of pyroptosis, and simultaneously reduce the autophagy level. Vitamin D alleviated high-glucose-induced pyroptosis (by suppressing GSDMD/NLRP3) and autophagic inhibition by activating the AMPK-mTOR axis (upregulating p-AMPK and downregulating mTOR), and improved lipid accumulation and hepatic sinusoidal capillarization. In the mouse model of MAFLD, VD supplementation can induce autophagy, inhibit pyroptosis and capillarization, and improve MAFLD. <b>Conclusions:</b> These results demonstrate, for the first time, that VD mitigates LSEC dysfunction through dual mechanisms: activating AMPK-dependent autophagy and inhibiting pyroptosis, providing a therapeutic rationale for VD in treating MAFLD-related sinusoidal pathology.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine Learning-Augmented Triage for Sepsis: Real-Time ICU Mortality Prediction Using SHAP-Explained Meta-Ensemble Models.","authors":"Hülya Yilmaz Başer, Turan Evran, Mehmet Akif Cifci","doi":"10.3390/biomedicines13061449","DOIUrl":"10.3390/biomedicines13061449","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Optimization algorithms are acknowledged to be critical in various fields and dynamical systems since they provide facilitation in identifying and retrieving the most possible solutions concerning complex problems besides improving efficiency, cutting down on costs, and boosting performance. Metaheuristic optimization algorithms, on the other hand, are inspired by natural phenomena, providing significant benefits related to the applicable solutions for complex optimization problems. Considering that complex optimization problems emerge across various disciplines, their successful applications are possible to be observed in tasks of classification and feature selection tasks, including diagnostic processes of certain health problems based on bio-inspiration. Sepsis continues to pose a significant threat to patient survival, particularly among individuals admitted to intensive care units from emergency departments. Traditional scoring systems, including qSOFA, SIRS, and NEWS, often fall short of delivering the precision necessary for timely and effective clinical decision-making. <b>Methods:</b> In this study, we introduce a novel, interpretable machine learning framework designed to predict in-hospital mortality in sepsis patients upon intensive care unit admission. Utilizing a retrospective dataset from a tertiary university hospital encompassing patient records from January 2019 to June 2024, we extracted comprehensive clinical and laboratory features. To address class imbalance and missing data, we employed the Synthetic Minority Oversampling Technique and systematic imputation methods, respectively. Our hybrid modeling approach integrates ensemble-based ML algorithms with deep learning architectures, optimized through the Red Piranha Optimization algorithm for feature selection and hyperparameter tuning. The proposed model was validated through internal cross-validation and external testing on the MIMIC-III dataset as well. <b>Results:</b> The proposed model demonstrates superior predictive performance over conventional scoring systems, achieving an area under the receiver operating characteristic curve of 0.96, a Brier score of 0.118, and a recall of 81. <b>Conclusions:</b> These results underscore the potential of AI-driven tools to enhance clinical decision-making processes in sepsis management, enabling early interventions and potentially reducing mortality rates.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.","authors":"Yixin Zhao, Jihan Wang, Lijuan Xu, Haofeng Xu, Yu Yan, Heping Zhao, Yuzhu Yan","doi":"10.3390/biomedicines13061443","DOIUrl":"10.3390/biomedicines13061443","url":null,"abstract":"<p><p>Osteoporosis is a systemic bone disorder characterized by decreased bone mass and deteriorated microarchitecture, leading to an increased risk of fractures. Recent studies have revealed that its pathogenesis involves complex biological processes beyond bone remodeling, including oxidative stress, chronic inflammation, cellular senescence, osteoimmunology, gut microbiota alterations, and epigenetic modifications. Oxidative stress disrupts bone homeostasis by promoting excessive free radical production and osteoclast activity. Chronic inflammation and the accumulation of senescent cells impair skeletal repair mechanisms. Advances in osteoimmunology have highlighted the critical role of immune-bone crosstalk in regulating bone resorption and formation. Moreover, the gut-bone axis, mediated by microbial metabolites, influences bone metabolism through immune and endocrine pathways. Epigenetic changes, such as DNA methylation and histone modification, contribute to gene-environment interactions, affecting disease progression. Multi-omics approaches (genomics, proteomics, and metabolomics) systematically identify molecular networks and comorbid links with diabetes/cardiovascular diseases, revealing pathological feedback loops that exacerbate bone loss. In conclusion, osteoporosis pathogenesis extends beyond bone remodeling to encompass systemic inflammation, immunometabolic dysregulation, and gut microbiota-host interactions. Future research should focus on integrating multi-omics biomarkers with targeted therapies to advance precision medicine strategies for osteoporosis prevention and treatment.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Inflammatory Effect of Pestalotic Acid A Derived from <i>Pestalotiopsis vismiae,</i> an Endophytic Fungus of <i>Ilex prenatal</i>, in Lipopolysaccharide-Stimulated RAW264.7 Cells.","authors":"Da Young Hwang, Dae-Won Ki, Dae-Cheol Choi, Bong-Sik Yun, Yoon Hee Kim","doi":"10.3390/biomedicines13061445","DOIUrl":"10.3390/biomedicines13061445","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Pestalotic acid A (PAA), a polyketide derived from <i>Pestalotiopsis vismiae</i>, an endophyte of the Japanese holly (<i>Ilex crenata</i>), is known to exhibit known antimicrobial activity, but its anti-inflammatory properties remain uncharacterized. This study aimed to investigate the anti-inflammatory effects of PAA in lipopolysaccharide (LPS)-stimulated murine macrophages, RAW264.7 cells. <b>Methods:</b> PAA was isolated from <i>P. vismiae</i> endophytes of <i>Ilex crenata,</i> and its structure was confirmed. RAW264.7 macrophages were treated with 0-50 μM of PAA in the presence of 100 ng/mL LPS. Cell viability was assessed by MTS assay; nitric oxide (NO) production was measured via Griess reagent; interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF) were quantified by enzyme-linked immunosorbent assay. Protein expression of inducible NO synthase (iNOS), nuclear factor (NF)-κB p65 phosphorylation, and related signaling proteins was evaluated by Western blot analysis and immunofluorescence staining. <b>Results:</b> PAA significantly increased macrophage viability and dose-dependently inhibited the release of NO by alleviating the protein expression of iNOS in LPS-treated RAW264.7 cells. Furthermore, PAA suppressed the release of IL-6, IL-1β, and TNF induced by LPS. Western blot and immunofluorescence results also indicated that PAA blocked the p65 subunit phosphorylation of NF-κB, which is one of the underlying mechanisms of the anti-inflammatory action of pestalotic acid A. <b>Conclusions:</b> PAA exerts potent anti-inflammatory effects in LPS-stimulated macrophages via inhibition of the NF-κB pathway, highlighting its potential as a natural therapeutic agent for inflammatory diseases.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12191257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional Enrichment Analysis of Rare Mutations in Patients with Brain Arteriovenous Malformations.","authors":"Elena Zholdybayeva, Ayazhan Bekbayeva, Karashash Menlibayeva, Alua Gusmaulemova, Botakoz Kurentay, Bekbolat Tynysbekov, Almas Auganov, Ilyas Akhmetollayev, Chingiz Nurimanov","doi":"10.3390/biomedicines13061451","DOIUrl":"10.3390/biomedicines13061451","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Brain arteriovenous malformations (bAVMs) are rare vascular anomalies characterized by direct connections between arteries and veins, bypassing the capillary network. This study aimed to identify potential genetic factors contributing to the development of sporadic bAVMs. <b>Methods</b>: Three patients (AVM1-3) from Kazakhstan who underwent microsurgical resection at the National Centre for Neurosurgery (NCN) in Astana, Kazakhstan, were analyzed. Brain AVMs were diagnosed using magnetic resonance imaging (MRI). Genomic DNA was isolated from whole venous blood samples, and whole-exome sequencing was performed on the NovaSeq 6000 platform (Illumina). Variants were filtered according to standard bioinformatics protocols, and candidate gene prioritization was conducted using the ToppGene tool. <b>Results</b>: In silico analysis further revealed candidate genes likely associated with lesion development, including COL3A1, CTNNB1, LAMA1, NPHP3, SLIT2, SLIT3, SMO, MAPK3, LRRK2, TTN, ERBB2, PARD3, and OBSL1. It is essential to focus on the genetic variants affecting the following prioritized genes: ERBB2, SLIT3, SMO, MAPK3, and TTN. Mutations in these genes were predicted to be \"damaging\". Most of these genes are involved in signaling pathways that control vasculogenesis and angiogenesis. <b>Conclusions</b>: Defects in genes associated with ciliary structure and function may be critical to the pathogenesis of brain AVMs. These findings provide valuable insights into the molecular underpinnings of bAVM development, emphasizing key biological pathways and potential candidate genes. Further research is needed to establish robust correlations between specific genetic mutations and clinical phenotypes, which could ultimately inform the development of improved diagnostic, therapeutic, and prognostic approaches.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12191260/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perimesencephalic Subarachnoid Hemorrhage Bleeding Patterns Are Not Always Benign: Prognostic Impact of an Aneurysmal Pathology.","authors":"Emily Hoffmann, Công Dùy Bui, David Ventura, Manfred Musigmann, Alexandra Valls Chavarria, Markus Holling, Vivek S Yedavalli, Jeremy J Heit, Christian Paul Stracke, Tobias D Faizy, Hermann Krähling, Burak Han Akkurt","doi":"10.3390/biomedicines13061444","DOIUrl":"10.3390/biomedicines13061444","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Perimesencephalic subarachnoid hemorrhage (pmSAH) is generally considered to be a benign variant of spontaneous SAH. However, in rare cases, an underlying aneurysm may be present, altering both clinical management and prognosis. The aim of this study was to evaluate the prognostic impact of aneurysmal pathology in patients presenting with perimesencephalic hemorrhage, focusing on the occurrence of complications and functional outcomes. <b>Methods</b>: This single-center, retrospective study included 77 patients diagnosed with perimesencephalic hemorrhage between 2012 and 2022. Clinical and radiological data were extracted, including demographics, risk factors, complications (hydrocephalus, vasospasm, and delayed cerebral ischemia (DCI)), and outcome scores (Glasgow Outcome Scale (GOS) and modified Rankin scale (mRS) at discharge). Patients were divided into two groups based on the presence or absence of an aneurysm confirmed through digital subtraction angiography (DSA). <b>Results</b>: Of the 77 patients, 7 (9.1%) were found to have an aneurysm. While rates of complications such as hydrocephalus and DCI were higher in the aneurysm group, these differences did not reach statistical significance. However, patients with aneurysms had significantly worse functional outcomes, with higher mRS and lower GOS scores at discharge. Logistic regression confirmed the presence of aneurysms as an independent factor associated with poor outcomes (OR = 21.6; 95% CI: 1.00-467.3; <i>p</i> = 0.050), while other variables such as age, sex, and World Federation of Neurosurgical Societies (WFNS) score were not statistically significant. ROC analysis showed moderate discriminative power of aneurysm presence for poor outcomes (AUC = 0.72). <b>Conclusions</b>: The presence of an aneurysm, although rare in pmSAH, significantly worsens functional outcomes. These findings highlight the necessity of early and sensitive vascular diagnostics-particularly DSA-to reliably exclude aneurysms. Differentiating between aneurysmal and non-aneurysmal perimesencephalic bleeding is essential not only for clinical decision-making but also for optimizing resource allocation in neurocritical care.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin Receptor Blockade Does Not Decrease Synthetic Angiotensin II (Giapreza^®) Effectiveness in Perioperative Hypotension Surrounding Kidney Transplant.","authors":"Natalie Pettit, Jamie Benken, Benito Valdepeñas, Nishita Gandhi, Rama Alyousef, Scott Benken","doi":"10.3390/biomedicines13061442","DOIUrl":"10.3390/biomedicines13061442","url":null,"abstract":"<p><p><b>Background/Objectives</b>: The use of angiotensin II (AT2S) as a vasopressor in patients receiving angiotensin receptor blockers (ARBs) prior to kidney transplant (KT) raises theoretical concerns. At our center, AT2S is the first-line vasopressor during KT. This study evaluated the hemodynamic and clinical effects of pre-transplant ARBs on AT2S use in KT. <b>Methods</b>: This single-center, retrospective cohort trial included patients with hypertension ≥ 18 years old on antihypertensive therapy who received AT2S as the first-line vasopressor peri-transplant. Patients were divided into ARB and non-ARB cohorts. Primary outcomes included total AT2S duration, time with SBP < 120 mmHg, and need for additional vasopressor support. <b>Results</b>: A total of 65 patients were analyzed: 22 in the ARB group and 43 in the non-ARB group. There were no significant differences in the frequency or duration of SBP < 120 mmHg or additional vasopressor requirements between groups (<i>p</i> > 0.05). Hospital and ICU stay length, safety, and adverse drug events were also similar. <b>Conclusions</b>: Contrary to theoretical concerns and observations in other distributive shock populations, no significant hemodynamic or clinical differences were observed in the response to AT2S in patients with pre-transplant ARB use.</p>","PeriodicalId":8937,"journal":{"name":"Biomedicines","volume":"13 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12190507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}