Microcirculation最新文献

{"title":"Observational Study of Sublingual Microcirculation in Patients With Chronic Cardiovascular Disease","authors":"Jacob Niculcea,&nbsp;James W. Schurr,&nbsp;Fatima M. Talebi,&nbsp;Joyce W. Wald,&nbsp;John C. Greenwood","doi":"10.1111/micc.70032","DOIUrl":"10.1111/micc.70032","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Sublingual video microscopy is increasingly used to study the microcirculation in acute illness. However, the sublingual microcirculation in patients with chronic cardiovascular diseases (CVD) is understudied. Our objective was to quantify sublingual microcirculatory parameters in a large cohort of patients with CVD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>One hundred and thirteen patients with CVD were enrolled. Incident dark-field handheld video microscopy (IDF-HVM) was used to quantify microvascular flow index (MFI), microvascular heterogeneity index (MHI), proportion of perfused vessels (PPV), perfused vessel density (PVD), and total vessel density (TVD). Data were stratified by age quartiles (20–39, 40–59, 60–79, 80+), cardiovascular comorbidities (hypertension, diabetes, chronic kidney disease, coronary artery disease, heart failure), and systemic hemodynamics (mean arterial pressure and pulse pressure).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In our 113 patient cohort, overall MFI = 2.86 ± 0.20; MHI = 0.15 ± 0.20; PPV = 94.3% ± 4.9%; PVD = 23.1 ± 4.7 mm/mm²; and TVD = 24.5 ± 4.8 mm/mm². Diabetic patients had lower mean MHI (0.10 vs. 0.17; <i>p</i> = 0.046) compared to those without diabetes. There was no difference in sublingual parameters attributable to other CVDs, age, or hemodynamics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In patients with stable cardiovascular disease, sublingual microvascular parameters are similar across age, blood pressure, and comorbidity cohorts, with the exception of decreased MHI in diabetic patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12517397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280529","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":"Effects of Different Isometric Exercise Modalities on Microvascular and Metabolic Function","authors":"Minyoung Kwak,&nbsp;Brian Benitez,&nbsp;Clara J. Mitchinson,&nbsp;Erik R. Snell,&nbsp;Haley C. Bergstrom","doi":"10.1111/micc.70031","DOIUrl":"10.1111/micc.70031","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study compared near-infrared spectroscopy (NIRS)-derived microvascular function, muscle oxygenation (SmO₂) dynamics, and fatigability during sustained isometric forearm flexion under two conditions: a rating of perceived exertion (RPE) level of 3 (RPE-Clamp) versus a constant torque (CT) matched to the torque produced during the first second of RPE-Clamp.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Thirteen healthy males (22.2 ± 4.7 year) completed both tasks on separate days. SmO₂ was measured during exercise, maximal voluntary isometric contractions (MVIC) were performed before and after exercise, and time to task failure (TTF) was recorded. Vascular occlusion tests (VOT) were used to assess microvascular function pre- and post-exercise.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CT induced significantly greater performance fatigability than RPE-Clamp (<i>p</i> &lt; 0.001), despite similar TTF (<i>p</i> = 0.171). SmO₂ significantly decreased during early (<i>p</i> = 0.001) and final (<i>p</i> = 0.028) phases of CT, while increasing during mid (<i>p</i> &lt; 0.001) phases in RPE-Clamp. Post-VOT indicated a significantly reduced desaturation rate (slope 1; <i>p</i> &lt; 0.001), a greater extent of tissue hypoxia (minimum SmO₂; <i>p</i> = 0.003), and increased microvascular reactivity (slope 2; <i>p</i> = 0.021) than pre-VOT, with greater peak re-saturation (MaxSmO₂; <i>p</i> = 0.010) observed in CT than RPE-Clamp.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Despite greater fatigability and desaturation in CT, both exercise modalities may enhance microvascular reactivity. Prolonged isometric exercise and subsequent hypoxic stress may contribute to a reduced desaturation rate post-exercise.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145280618","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":"Apolipoprotein M (ApoM) Ameliorates Acute Alcohol Intoxication (AAI)-Hemorrhagic Shock and Resuscitation (HSR)-Induced Microvascular Leakage","authors":"Mengmeng Chang,&nbsp;Jerome W. Breslin","doi":"10.1111/micc.70030","DOIUrl":"https://doi.org/10.1111/micc.70030","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Microvascular hyperpermeability is a serious complication that occurs from hemorrhagic shock and resuscitation (HSR), especially when combined with acute alcohol intoxication (AAI). We tested the hypothesis that administration of Apolipoprotein M (ApoM), a lipocalin that normally resides in plasma high-density lipoproteins (HDL) and a carrier of sphingosine-1-phosphate (S1P), reduces combined AAI and HSR-induced microvascular leakage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>An established rat model of AAI/HSR was combined with intravital microscopy to study whether the administration of ApoM in resuscitative fluids reduces microvascular leakage of FITC-albumin. The impact of ApoM on human umbilical vein endothelial cell (HUVEC) monolayer barrier function and junctional integrity was tested, using trans-endothelial electrical resistance (TER) and immunofluorescence labeling of junctional VE-Cadherin, respectively. Immunoprecipitation of ApoM in HUVEC and mass spectrometry of complexes were used to determine potential binding partners. The Rac1 G-LISA assay was used to determine if ApoM causes Rac1 activation in HUVEC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared to sham controls, combined AAI and HSR significantly increased microvascular leakage. Administration of S1P, ApoM, or their combination during resuscitation significantly decreased microvascular leakage. In HUVEC monolayers, with or without alcohol pretreatment, S1P, ApoM, and S1P + ApoM all significantly increased barrier function and improved the junctional integrity of VE-cadherin compromised by alcohol. The small GTPase Rac1 was found to bind with ApoM in HUVEC and was significantly activated within 5 min of ApoM addition.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The findings suggest that fluid resuscitation with ApoM ameliorates AAI/HSR-induced microvascular leakage. The mechanism involves stabilizing VE-Cadherin junction integrity, which could be caused by Rac1 activation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145272455","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":"Shear Stress Regulates ABCA1-Dependent Membrane Cholesterol Content in Endothelial Cells Facilitating H2S-Dependent Vasodilation","authors":"Jacob R. Anderson,&nbsp;Nancy L. Kanagy,&nbsp;Laura V. Gonzalez Bosc,&nbsp;Jay S. Naik","doi":"10.1111/micc.70029","DOIUrl":"10.1111/micc.70029","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>Endothelial cells (ECs) express an array of integral membrane proteins, including ion channels and transporters that contribute to blood flow regulation and cell–cell communication. Many of these membrane proteins are regulated by plasma membrane cholesterol content. The ATP-binding cassette family A1 (ABCA1) transporter is a regulator of membrane cholesterol content. We have shown increased ABCA1 mRNA expression and reduced EC membrane cholesterol in resistance mesenteric arteries compared to conduit arteries. Previous studies suggest shear stress (SS) can increase or decrease ABCA1 expression in a cell-type-dependent manner.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Hypothesis</h3>\u0000 \u0000 <p>SS sustains lower EC membrane cholesterol concentration through ABCA1-mediated cholesterol transport, facilitating H₂S-mediated vasodilation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The effect of SS on ABCA1 and membrane cholesterol content was assessed in pressurized mesenteric arteries from male Sprague–Dawley rats and cultured human aortic endothelial cells. Pressure myography was used to assess the effects of ABCA1 inhibition on H₂S-mediated vasodilation. Filipin was used to assess EC membrane cholesterol content.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>SS increased ABCA1 expression in the endothelium of mesenteric arteries and cultured human aortic endothelial cells and markedly reduced EC membrane cholesterol. Inhibition of ABCA1 increased EC membrane cholesterol content and abolished H₂S-induced vasodilation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>SS facilitation of EC-dependent vasodilation appears to be mediated by membrane cholesterol content.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12498007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145232828","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":"CaMKII Antagonism Improves Vascular Dysfunction in the Visceral Adipose Microvasculature of Obese Subjects.","authors":"Bulbul Ahmed, Melissa G Farb, Sophia D'Alessandro, Luise Pernar, Brain Carmine, Donald T Hess, Kenneth Walsh, Noyan Gokce","doi":"10.1111/micc.70033","DOIUrl":"https://doi.org/10.1111/micc.70033","url":null,"abstract":"<p><strong>Objective: </strong>We have previously demonstrated angiogenic impairment, inflammation, and endothelial vasomotor dysfunction in the visceral adipose vasculature of obese individuals. Here, we investigated the role of calcium/calmodulin-dependent protein kinase II (CaMKII) in the regulation of vascular phenotype in the adipose microvasculature.</p><p><strong>Methods: </strong>Using visceral and subcutaneous fat specimens biopsied from obese subjects (BMI 48 ± 9 kg/m², age 38 ± 11 years), we examined the effect of CaMKII antagonism on acetylcholine-mediated, endothelium-dependent vasodilation of isolated arterioles using videomicroscopy and studied angiogenic capillary sprouting capacity ex vivo.</p><p><strong>Results: </strong>Pharmacological inhibition of CaMKII with KN-93 improved endothelium-dependent vasodilation of isolated visceral arterioles by 3-fold (p < 0.001 vs. control) and increased visceral fat sprouting capacity by 2.5-fold (p < 0.001). Inhibition of endothelial nitric oxide synthase with N(ω)-nitro-l-arginine methyl ester blunted KN-93-induced improvements in vasodilation and angiogenesis, suggesting dependence on increased nitric oxide bioavailability. KN-93 had no effect on subcutaneous angiogenic capacity, which exhibited preserved angiogenic growth compared to visceral fat. KN-93 exposure was associated with reduced reactive oxygen species generation and decreased vascular gene expression of JUN, NFAT5, and CAMKII signaling components.</p><p><strong>Conclusion: </strong>Our findings suggest that CaMKII signaling may negatively modulate microvascular function, contribute to increased oxidative stress, and pro-inflammation observed in the visceral adipose microenvironment in obesity.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":"e70033"},"PeriodicalIF":2.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145345969","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":"Volumetric Analysis of the Blood–Brain Barrier After Ischemic Stroke by Electron Tomography in Mice","authors":"Pavel Kotchetkov,&nbsp;Baptiste Lacoste","doi":"10.1111/micc.70025","DOIUrl":"https://doi.org/10.1111/micc.70025","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Transmission electron microscopy (TEM) enables ultrastructural investigation of both organic and nonorganic samples. However, conventional TEM is limited by the acquisition of two-dimensional snapshots, restricting our volumetric understanding of complex ultrastructures. Electron tomography (ET) overcomes this limitation by offering detailed three-dimensional (3D) specimen representation. ET has been widely applied in biology; however, its use for blood–brain barrier (BBB) assessment has been overlooked. The BBB ensures proper brain function by limiting the entrance of blood-borne molecules into the brain and ensuring selective transport. The BBB is disrupted in several pathological conditions, resulting in neuronal damage. Understanding the fine changes underlying BBB disruption requires advanced imaging tools such as ET.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We developed a detailed room temperature electron tomography (RT-ET) method for sample preparation, tomogram generation, 3D segmentation, and applied this approach to assess ultrastructural changes in brain endothelial cells (ECs) after photothrombotic stroke in mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our findings identify altered transcytotic vesicle morphology, as well as remodeling of the endoplasmic reticulum, indicative of cellular stress and impaired vesicular trafficking.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our toolkit allows for reproducible, high-resolution analysis of brain microvascular pathology. This new RT-ET approach uncovers previously inaccessible ultrastructural alterations in ECs following ischemic stroke in mice, offering new insight into mechanisms of BBB disruption.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102296","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":"Blood Flow Simulation and Uncertainty Quantification in Extensive Microvascular Networks: Application to Brain Cortical Networks","authors":"Peter Mondrup Rasmussen","doi":"10.1111/micc.70027","DOIUrl":"https://doi.org/10.1111/micc.70027","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Microvascular blood flow simulations enhance understanding of microcirculatory phenomena at the micrometer scale by capturing heterogeneity in blood flow. However, imaged areas often only partially represent tissue regions, leading to numerous vessels crossing boundaries and strongly influencing simulated blood flows through imposed boundary conditions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Two key methodological aspects of blood flow simulations are addressed: selecting appropriate boundary conditions and quantifying the inevitable impact of boundary condition uncertainties on model simulations. An adaptive method for pressure boundary conditions is proposed and rigorously evaluated in extensive brain cortical microvascular networks. The adaptive method is integrated into a Bayesian calibration framework, inferring distributions over thousands of unknown pressure boundary conditions and providing uncertainty estimates for model simulations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The adaptive method produces simulations consistent with reference data, yielding depth-dependent pressure drop profiles and layer-wise capillary blood flow profiles consistent with previous analysis. These hemodynamic phenomena generalize to biphasic blood flow simulation models incorporating in vivo viscosity formulations. Uncertainty quantification reveals a novel spatially heterogeneous and depth-dependent pattern in blood flow uncertainty.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The adaptive method for pressure boundary conditions will be useful in future applications of both forward and inverse blood flow simulations. Uncertainty quantification complements hemodynamic predictions with associated uncertainties.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102295","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":"Vasoactive Intestinal Peptide: Another Player in Adipose Tissue Blood Flow Regulation?","authors":"Richard Sotorník,&nbsp;Julie Ménard,&nbsp;Pascal Brassard,&nbsp;Maude Gagnon-Auger,&nbsp;Jean-Patrice Baillargeon,&nbsp;Jean-Luc Ardilouze","doi":"10.1111/micc.70026","DOIUrl":"https://doi.org/10.1111/micc.70026","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>In healthy people, adipose tissue blood flow (ATBF) rises postprandially; however, in one third of them, this response is altered. These people are characterized by prolonged postprandial lipemia and higher cardiometabolic risk. Vasoactive intestinal peptide (VIP) is a gut neurotransmitter with a vasodilatory effect. The aim of the study was to assess the role of VIP in ATBF regulation and its postprandial blunting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Plasma VIP and ATBF (¹³³Xenon washout technique) were measured during a 75 g oral glucose load in 16 healthy participants. ATBF was monitored in 12 individuals during in situ microinfusion of incremental doses of VIP (10⁻⁷, 10⁻⁶, 10⁻⁵ mol L⁻¹).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Oral glucose induced no change in plasma VIP. Post-glucose ATBF measures identified 7 non-responders (peak blood flow &lt; 50% of fasting values) and 9 responders. Compared to baseline (2.50 [1.96–3.59] mL·100 g⁻¹ min⁻¹), local microinfusion of VIP increased ATBF dose-dependently: 2.67 [2.18–3.89]; 4.35 [3.33–4.65]; and 7.91 [6.59–9.88] mL·100 g⁻¹ min⁻¹ (<i>p</i> &lt; 0.0001) with a non-significant lower response to VIP in non-responders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings show a potent vasodilatory effect of VIP in adipose tissue and suggest that individuals with a blunted ATBF response to glucose load have a lower response. Whether the local unresponsiveness to VIP participates in this non-responder status has to be confirmed in larger studies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145057933","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":"Satellite Cell Ablation Limits Myofiber Regeneration but Not Angiogenesis Following Skeletal Muscle Injury","authors":"Nicole L. Jacobsen,&nbsp;Michael A. Nguyen,&nbsp;Aaron B. Morton,&nbsp;DDW Cornelison,&nbsp;Steven S. Segal","doi":"10.1111/micc.70024","DOIUrl":"https://doi.org/10.1111/micc.70024","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Myotoxin injury of skeletal muscle disrupts myofibers and fragments capillaries. Following injury, myofibers and capillaries regenerate in concert; however, it remains unresolved whether myogenesis and angiogenesis are interdependent processes. We tested the hypothesis that myofiber regeneration is required for revascularization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>To limit myofiber regeneration, satellite cells were depleted by tamoxifen injections (+TMX) in adult <i>Pax7-Cre</i>^{ERT2<i>/+</i>}; <i>Rosa</i>^DTA<i>/+</i> (Pax7-DTA) mice; vehicle injections (−TMX) served as controls. Two weeks later, the gluteus maximus muscle was injured by local injection of BaCl₂. Regeneration of myofibers and microvessels was assessed histologically. Microvascular perfusion was evaluated with fluorescent tracers injected into the bloodstream.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Myofiber regeneration was minimal in +TMX. Through 21 days post injury (dpi), microvascular area (CD31 immunostaining) was similar between +TMX and −TMX, with disoriented microvessels prevailing in +TMX. At 7 dpi, fewer capillaries were perfused in +TMX compared to −TMX. At 21 dpi, EC area and capillary perfusion were not different between groups. For +TMX at 28 dpi, distinct regions with fewer perfused microvessels near “ghost” fibers were accompanied by adjacent areas of robust vascularity and clusters of adipocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Following myotoxin injury after satellite cell ablation, angiogenesis ensues without myogenesis, and the microcirculation remodels according to changes in tissue composition.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145057810","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":"Dual Disruption of Embryonic Angiogenesis by Hyperglycemia: Structural and Hemodynamic Alterations Revealed via OCT Angiography and Biospeckle Imaging in the Chick CAM Model","authors":"Abhishek Banerjee,&nbsp;Avinash Kumar,&nbsp;Raju Poddar","doi":"10.1111/micc.70023","DOIUrl":"https://doi.org/10.1111/micc.70023","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigates the effects of hyperglycemia on vascular morphology and hemodynamics during embryogenesis using the chick chorioallantoic membrane (CAM) model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We employed a dual-modality, label-free imaging approach, Optical Coherence Tomography Angiography (OCTA) and biospeckle imaging, to evaluate microvascular architecture and real-time flow dynamics in chick embryos subjected to hyperglycemic conditions. Quantitative metrics such as vessel area, branching junctions, lacunarity, and biospeckle contrast were analyzed to assess angiogenic and metabolic responses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Hyperglycemia caused significant vascular attrition, including a 31% reduction in vessel area, 55% fewer vascular junctions, and a 58% increase in lacunarity, indicating fragmented and simplified networks. Biospeckle imaging revealed reduced blood flow velocities and elevated non-vascular speckle contrast, suggestive of metabolic stress and endothelial apoptosis. These vascular impairments extended to the retina, where hyperglycemic embryos exhibited thinner retinas, smaller lenses, and sparser retinal vasculature.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings demonstrate that embryonic hyperglycemia leads to widespread vascular simplification and hemodynamic dysfunction, driven by oxidative stress and disrupted VEGF signaling. Unlike adult diabetic vasculopathy, the embryonic response involves global, not focal, vascular defects. This work establishes a novel multimodal imaging framework for studying developmental angiogenesis and lays the groundwork for future investigations into therapeutic strategies targeting diabetic embryopathy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 7","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923849","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}