Microcirculation最新文献

{"title":"Quantification of Lacteal Contractility by Live Intravital Imaging","authors":"Majid Mufaqam Syed-Abdul","doi":"10.1111/micc.70080","DOIUrl":"10.1111/micc.70080","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Lacteal motion can be visualized in vivo, but quantitative analysis remains difficult because intravital intestinal imaging is affected by motion, focal instability, and baseline fluorescence variability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We developed an intravital imaging workflow for quantitative analysis of lacteal contractility in Prox1-EGFP rats. Lacteals were segmented by region-of-interest analysis, and fluorescence signals were extracted frame by frame. Signals were normalized as percent deviation from mean clip intensity. Contractility was assessed from normalized traces, with acetylcholine used as a positive control. Matched 30 and 10 s analysis windows were compared.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Mean-normalized signals provided a more comparable readout than raw intensity across clips acquired under variable intravital conditions. The workflow detected the expected increase in lacteal contractile behavior after acetylcholine in paired experiments and resolved progressive augmentation in a serial time-course experiment. Compared with 10 s analysis, 30 s recordings yielded a more coherent and interpretable amplitude-based readout.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study establishes a practical intravital workflow for quantifying lacteal contractility in vivo and defines key analytical considerations for live intestinal imaging, including normalization strategy, window selection, and image-quality control.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148605056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Viral Control: Tenofovir's Hidden Impact on Blood–Brain Barrier Endothelial Cells","authors":"Saarah Behardien,&nbsp;Khayelihle Brian Makhathini,&nbsp;Chontrelle Willemse,&nbsp;David Fisher","doi":"10.1111/micc.70079","DOIUrl":"10.1111/micc.70079","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>The blood–brain barrier (BBB) is a dynamic endothelial interface that protects the brain from harmful agents while regulating molecular exchange. Human immunodeficiency virus (HIV) compromises BBB integrity, promoting neurological damage. Antiretroviral (ARV) therapies suppress HIV replication, preventing immune system deterioration and progression to AIDS. Although Tenofovir-based ARV regimens are vital for HIV treatment and prevention, their impact on cerebrovascular function remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>This study examined Tenofovir's effects on murine brain endothelial cells using an in vitro BBB model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Brain endothelial cells (bEnd.5) were treated with Tenofovir Disoproxil Fumarate (TDF; 9.8–98 ng/mL) or Tenofovir Alafenamide (TAF; 1–10 ng/mL) for 24–96 h. Cell proliferation, cell cycle progression (via flow cytometry) and monolayer permeability (via Transendothelial Electrical Resistance) were evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Both TDF and TAF treatments suppressed cell division by S-phase disruption of the cell cycle and increased monolayer permeability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that prolonged TDF or TAF exposure compromises BBB integrity by inhibiting endothelial cell division and altering barrier function, which could have implications for HIV-ARV-induced neurodegeneration in individuals receiving long-term Tenofovir-based therapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70079","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148376333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carbon Dioxide Concentration Alters the Dynamics of Oxygen-Mediated Capillary Blood Flow Responses in Skeletal Muscle","authors":"Alexander Folkins,&nbsp;Gaylene M. Russell McEvoy,&nbsp;Graham M. Fraser","doi":"10.1111/micc.70075","DOIUrl":"10.1111/micc.70075","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Hypothesis</h3>\u0000 \u0000 <p>We hypothesize that the dynamics of O₂-mediated blood flow responses in skeletal muscle capillaries are altered under different tissue carbon dioxide concentrations ([CO₂]) due to the interaction of overlapping mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Eight male Sprague Dawley rats (164–215 g) were anesthetized and instrumented for systemic monitoring. The extensor digitorum longus muscle was isolated and reflected over a microfluidic gas exchange chamber mounted in an inverted microscope stage. 4-min intravital video recordings of capillary blood flow during O₂ challenges consisted of a 1-min baseline at 7% O₂ concentration ([O₂]), followed by 3 min at 2% [O₂], under constant background [CO₂] at 2%, 5%, and 8%. Recordings were analyzed offline using custom MATLAB software. Time transients (τ) of capillary hemodynamic responses were determined using a least squared regression fit to single- and double-exponential models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Fast component τ of the O₂-mediated capillary red blood cell (RBC) velocity response was 2.1 s for 2% [CO₂], 3.8 s for 5% [CO₂], and 7.0 s for 8% [CO₂]. Third minute low [O₂] capillary RBC supply rate increases from baseline were greater for 8% [CO₂] (5% [CO₂]: 6.4 ± 8.7 cells/s vs. 8% [CO₂]: 8.5 ± 10.7 cells/s, <i>p</i> = 0.0007).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The fast component τ of O₂-mediated capillary hemodynamic responses was found to be slower with increasing background tissue [CO₂], suggesting that multiple interacting mechanisms are involved to appropriately regulate O₂ delivery under different CO₂ conditions in partial support of the hypothesis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes Upregulates BKCa Channels in Pulmonary Arterial Smooth Muscle by Altering the Local Control Mechanism of the Pore-Gate Domain","authors":"Vadym Sydorenko,&nbsp;Irina Ivanova,&nbsp;Dariia Dryn,&nbsp;Mariia Melnyk,&nbsp;Oleksiy Boldyriev,&nbsp;Anatoly Soloviev","doi":"10.1111/micc.70077","DOIUrl":"10.1111/micc.70077","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Large conductance calcium-activated potassium channels (BK_Ca) play an important role in the regulation of vascular tone. However, the properties of BK_Ca channels in smooth muscle of pulmonary arteries are poorly understood. Previous experimental studies demonstrated that pulmonary hypoxic vasoconstriction as a normal physiological response to decreased oxygen levels was impaired in diabetic animals due to abnormal activation of BK_Ca channels. The aim of this study was to identify mechanisms of diabetes-induced activation of BK_Ca channels in freshly isolated smooth muscle cells from rat pulmonary arteries.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Type 1 diabetes was induced by streptozotocin (STZ). Whole-cell potassium currents were recorded using the patch-clamp method. Expression levels of BK-α and BK-β1 subunits were measured by real-time PCR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our results demonstrate that the amplitude of whole-cell current through BK_Ca channels in rat pulmonary artery smooth muscle cells is significantly increased during STZ-induced diabetes without altering the expression of BK-α and BK-β1 subunits and channel calcium sensitivity. The slow component of BK_Ca current deactivation time constant and spontaneous transient outward current amplitude were increased in diabetic animals compared to healthy animals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We conclude that abnormal activation of the BK_Ca channel in pulmonary arterial smooth muscle during diabetes is associated with alterations in the local control mechanism of the BK_Ca pore-gate domain.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Red Blood Cell Biomechanics in the Setting of Cancer-Associated Anemia and Chemotherapy","authors":"Deirdre Finnigan,&nbsp;Nick Cruickshanks,&nbsp;George Ilbawi,&nbsp;Regan Bucciol,&nbsp;Yousra Tera,&nbsp;Maha Othman","doi":"10.1111/micc.70074","DOIUrl":"https://doi.org/10.1111/micc.70074","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Red blood cells (RBCs) possess distinct biomechanical properties that enable their survival and efficient oxygen delivery. Cancer-associated anemia, frequently compounded by chemotherapy, is a major clinical challenge, yet little is known about how RBC biomechanics contribute to its pathophysiology. This study evaluates the biomechanical properties of RBCs in patients with cancer compared to controls and within patients before and after chemotherapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Biomechanical properties of RBCs were assessed in 110 women with breast, ovarian, or endometrial cancer, measured before and after chemotherapy, and compared findings with 35 healthy female controls. Thirteen biomechanical parameters were assessed using the MIZAR automated rheometer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Relative to controls, pre-chemotherapy cancer patients exhibited significantly higher RBC aggregation and elasticity. Within the cancer cohort, anemic patients demonstrated more deformable and elastic RBCs, with increased aggregation compared to non-anemic patients. Following chemotherapy, patients displayed reduced RBC deformability but further increased elasticity, consistent with chemotherapy-induced alterations to membrane structure and function; these effects were most pronounced in anemic patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We report novel rheological observations indicating that both cancer and chemotherapy are associated with alterations in RBC biomechanics, and that anemia further amplifies these changes. Importantly, cancer-associated anemia appears to involve impaired RBC quality. Recognition of biomechanical dysfunction may provide new insights into the mechanisms of cancer-related anemia and support the development of more comprehensive diagnostic and management strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148324844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZEB1 Modifies VE-Cadherin Signaling in Lymphatic Endothelial Cells","authors":"Nada S. Ahmed,&nbsp;Joseph L. Horder,&nbsp;Charles T. Cresswell,&nbsp;Poppy E. Harris,&nbsp;Amy P. Lynch,&nbsp;Zarah B. Tabrizi,&nbsp;Kathryn R. Green,&nbsp;James H. Hallwood,&nbsp;Anton C. Smith,&nbsp;Michael A. Portelli,&nbsp;Alexander J. Fezovich,&nbsp;Christos Spanos,&nbsp;David S. Gardner,&nbsp;Alan McIntyre,&nbsp;Sarah J. Storr,&nbsp;Daniel G. Booth,&nbsp;David O. Bates,&nbsp;Andrew V. Benest","doi":"10.1111/micc.70076","DOIUrl":"https://doi.org/10.1111/micc.70076","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Zinc finger E-box-binding homeobox 1 (ZEB1) is a transcription factor primarily known for its regulatory roles in epithelial-to-mesenchymal transition (EMT) and cell fate determination. Recent studies suggest that endothelial ZEB1 signaling promotes blood vessel growth and reduces junctional integrity, although the underlying mechanisms remain unclear. Notably, the role of ZEB1 in the lymphatic vasculature is unknown, and the regulation of lymphatic integrity by VE-cadherin remains poorly defined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Here, using an integrated proteomic and transcriptomic approach, we identify ZEB1-dependent signaling pathways associated with cell–cell junction reorganization in lymphatic endothelial cells (LECs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Loss of ZEB1 reduced VE-cadherin phosphorylation at pY731 and pY685 and was accompanied by decreased monolayer resistance and impedance, together with increased leukocyte transendothelial migration. ZEB1 knockdown also reduced YES tyrosine kinase expression and altered YAP1 expression and junctional localisation, changes that were associated with reduced VE-cadherin phosphorylation. Silencing YAP1 in HDLECs similarly reduced VE-cadherin phosphorylation and impaired barrier integrity, recapitulating aspects of the phenotype observed following ZEB1 knockdown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Collectively, these findings suggest that ZEB1 contributes to lymphatic endothelial barrier maintenance in association with altered YAP1 and YES signaling.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148324511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anisodamine Hydrobromide Ameliorates Pulmonary Microcirculatory Dysfunction in Septic Rats","authors":"Yan-Chen Liu,&nbsp;Ting-Ting Xie,&nbsp;Xiao-Yi Wang,&nbsp;Chong Yang,&nbsp;Xin-Xin Zhang,&nbsp;Qian-Zan Liao,&nbsp;Zheng Wang,&nbsp;Fan-Kai Chen,&nbsp;An-Qing Li,&nbsp;Ding-Zhou Weng,&nbsp;Jing-Yan Han,&nbsp;Jian Liu","doi":"10.1111/micc.70071","DOIUrl":"10.1111/micc.70071","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Pulmonary microcirculatory dysfunction is a hallmark of sepsis, contributing to hypoxemia, pulmonary edema, and multiple organ failure. Anisodamine hydrobromide (ADM), a natural alkaloid with anti-inflammatory and endothelial-protective properties, has been used clinically in China for septic shock. However, its effects on pulmonary microcirculatory dysfunction in septic shock remain unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A rat model of sepsis was established via cecal ligation and puncture (CLP). Rats were treated with low, medium, or high doses of ADM. Seven-day survival rates and arterial blood gas parameters were monitored. Pulmonary microvascular leakage was evaluated using Evans blue extravasation and FITC–dextran imaging. Histological analysis, immunofluorescence, and Western blotting were performed to assess leukocyte adhesion, inflammatory cell infiltration, endothelial junction proteins, basement membrane proteins, and matrix metalloproteinases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>ADM treatment significantly improved 7-day survival and restored arterial partial pressure of oxygen (PaO₂), oxygen saturation (SaO₂), and pH in CLP rats. High-dose ADM markedly reduced Evans blue and FITC-dextran leakage, attenuated pulmonary edema, and preserved alveolar architecture. ADM inhibited leukocyte adhesion in pulmonary microvessels and decreased infiltration of MPO- and CD68-positive inflammatory cells. Mechanistically, ADM suppressed CLP-induced Caveolin-1 upregulation, restored the expression of VE-Cadherin, Occludin, and Claudin-5, and prevented degradation of Collagen IV and Laminin. Additionally, ADM significantly downregulated MMP-9 expression, while MMP-2 levels remained unchanged, suggesting a role in limiting junctional and basement membrane degradation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>ADM protects against CLP-induced pulmonary microcirculation dysfunction in rats by attenuating inflammatory cell infiltration, preserving pulmonary endothelial junctions, and maintaining basement membrane integrity. These results provide mechanistic insight into ADM's therapeutic potential in sepsis-induced pulmonary microcirculation dysfunction and support its use for sepsis in clinic.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Relationship Between Sublingual Microcirculatory Structure and Frailty in Renal Transplant Candidates: Exploring Tortuosity & Endothelial Glycocalyx Biomarkers","authors":"Ryan A. P. Homes,&nbsp;Trent Payne,&nbsp;Fiona Giddens,&nbsp;Ross S. Francis,&nbsp;Ruth E. Hubbard,&nbsp;Emily H. Gordon,&nbsp;Mark J. Midwinter","doi":"10.1111/micc.70072","DOIUrl":"10.1111/micc.70072","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigated the relationship between sublingual microcirculatory tortuosity, frailty index scores, and endothelial glycocalyx blood biomarkers in individuals with chronic kidney disease (CKD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Sublingual microcirculatory videos were analyzed using a 0–4 tortuosity scoring scale. Plasma concentrations of syndecan-1 and soluble thrombomodulin were quantified using enzyme-linked immunosorbent assay (ELISA). Frailty status was assessed using a short-form frailty index questionnaire.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The study included 44 patients (median age 53 years, IQR 45–64) attending a kidney transplant assessment clinic, with equal representation of males and females. The median frailty index was 0.19 (IQR: 0.15–0.30), with 63.5% of participants having an FI score &lt; 0.25. Intraclass correlation coefficient (ICC) analysis demonstrated excellent inter-observer reliability for tortuosity scoring. Frailty index scores were significantly higher in participants with tortuosity scores of 3/4 compared to those with a score of 0. No significant differences were observed in syndecan-1 or soluble thrombomodulin levels across tortuosity scores. Ordinal logistic regression identified frailty index score as the only significant predictor of tortuosity, independent of age, dialysis type, or sex.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Higher frailty index scores were associated with increased sublingual microcirculatory capillary tortuosity, though this relationship did not extend to endothelial glycocalyx biomarkers. These findings highlight the potential value of incorporating tortuosity assessment alongside density and perfusion measures in microcirculatory evaluation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70072","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148157256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The British Microcirculation & Vascular Biology Society: Abstracts of the 75th Annual Meeting, Hosted by the University of Surrey, UK","authors":"","doi":"10.1111/micc.70061","DOIUrl":"https://doi.org/10.1111/micc.70061","url":null,"abstract":"","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148146999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLP-1 Receptors Are Enriched in the Lymphatic Endothelium and Their Pharmacological Activation With Semaglutide Improves the Pumping Capacity of Lymphatic Vessels","authors":"Mary E. Schulz,&nbsp;Victoria L. Akerstrom,&nbsp;Joseph H. Dayan,&nbsp;Jorge A. Castorena-Gonzalez","doi":"10.1111/micc.70070","DOIUrl":"https://doi.org/10.1111/micc.70070","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Recent clinical studies have suggested that glucagon-like peptide-1 receptor (GLP-1R) agonists may be effective therapies to treat or reduce the risk of developing secondary lymphedema. In this study, we aimed to (1) determine if GLP-1Rs are present in the lymphatic vasculature and characterize their expression, and (2) assess the effects of GLP-1R agonism on the contractile function of collecting lymphatic vessels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We assessed the expression of GLP-1Rs in and around the lymphatic vasculature by single-cell RNA sequencing and fluorescence confocal microscopy, and evaluated the direct effects of GLP-1R agonist, semaglutide, on modulating lymphatic contractility using pressure myography.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Expression of <i>Glp1r</i> (encoding GLP-1Rs) was detected exclusively in lymphatic endothelial cells. Pharmacological activation of GLP-1Rs led to robust vasodilation and an increase in the pumping capacity of isolated collecting lymphatics from WT, diet-induced obese, and hypercholesterolemic ApoE KO mice. The GLP-1R-mediated response was in part facilitated by nitric oxide and its potential interaction with NaV channels; however, additional signaling remains to be elucidated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our results revealed a direct, beneficial effect of GLP-1R agonism on lymphatic pumping capacity mediated by robust vasodilation, allowing lymphatics to accommodate and displace larger fluid volumes while maintaining strong and highly efficient contractions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 5","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148147043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}