Microcirculation最新文献

{"title":"Insights Into Remote Ischemic Conditioning miRNA Effects on Brain Endothelial Cells During Ischemia-Reperfusion.","authors":"Katrine Tang Stenz, Jesper Just, Zenghui Huang, Thomas Ravn Lassen, Kristian Vissing, Xiu-Jie Wang, Kim Ryun Drasbek","doi":"10.1111/micc.70060","DOIUrl":"10.1111/micc.70060","url":null,"abstract":"<p><strong>Objective: </strong>Acute ischemic stroke (AIS) is one of the leading causes of death and disabilities, and as such, it is of utmost importance to identify novel treatment options. Remote ischemic conditioning (RIC) is a promising non-invasive treatment that is thought to activate the body's own protective mechanisms against damaging ischemia. Here, we study the transcriptomic impact of microRNAs (miRNAs) that are upregulated by RIC.</p><p><strong>Methods: </strong>Using RNA sequencing, we investigated the transcriptional changes in human brain microvascular endothelial cells (HBMECs) transfected with four selected RIC-upregulated miRNAs (RIC-miRNAs), miR-16-5p, miR-144-3p, miR-182-5p, and miR-451a, under oxygen and glucose deprivation (OGD) and reoxygenation-mimicking the initial stages of AIS.</p><p><strong>Results: </strong>Pronounced transcriptional changes were present after RIC-miRNA transfection, with 149 unique downregulated and 212 upregulated differentially expressed genes in HBMECs after OGD and RIC-miRNA transfection compared to all other conditions. These genes were involved in pathways of energy metabolism and cell cycle regulation.</p><p><strong>Conclusion: </strong>Our study suggests that the selected RIC-miRNAs regulate pathways that may facilitate endothelial cell survival, recovery, and remodeling events from ischemic damage, adding to the knowledge of the pathways affected by RIC during stroke.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 4","pages":"e70060"},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817141","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":"Capillary Density and Neuronal Homeostasis in Human Primary Visual Cortex.","authors":"Yi-Chung Wang, Amy Guo, Adam J H Newton, Robert A McDougal, William W Lytton, Marcello M DiStasio","doi":"10.1111/micc.70064","DOIUrl":"10.1111/micc.70064","url":null,"abstract":"<p><strong>Background: </strong>Hypoxia is a critical determinant of neuronal function and vulnerability in the brain. While neuronal density has been extensively characterized across cortical regions, the spatial relationship between neurons and the microvasculature represents an additional structural constraint on oxygen diffusion and metabolic support. In particular, the distance between neurons and nearby capillaries influences local oxygen availability required to sustain neuronal activity and maintain ionic homeostasis.</p><p><strong>Methods: </strong>In this study, we quantified neuron-capillary spatial relationships across cortical layers in the human primary visual cortex. Postmortem tissue from three neuropathologically normal individuals (ages 55-75 years) was analyzed using dual-label immunohistochemistry for NeuN (neurons) and CD34 (vascular endothelial cells). Regions of interest corresponding to neocortical layers were delineated by a neuropathologist. Automated image analysis in QuPath was used to segment neurons using object-based classification and capillaries using pixel-based classification. Distances between neuronal and vascular centroids were corrected for tissue shrinkage using a linear scaling factor of 1.20. Centroids of segmented objects were extracted, and nearest-neighbor relationships were computed using a quad tree spatial search algorithm.</p><p><strong>Results: </strong>Across more than 155 000 neurons and 84 000 vascular objects, we observed a consistent laminar gradient in neuron-capillary distance. Neurons in superficial and deep layers were located farther from capillaries, whereas neurons in the central layers exhibited shorter distances, with layers III and IV demonstrating median distances of ~30-45 μm.</p><p><strong>Conclusions: </strong>These findings demonstrate that neuron-capillary spatial relationships vary systematically across cortical depth, suggesting that cortical microvascular architecture is consistent with layer-specific metabolic demands.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 4","pages":"e70064"},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147931095","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":"Adipose Triglyceride Lipase and Gpr40 Contribute to the Anti-Contractile Effect of Perivascular Adipose Tissue.","authors":"Miranda Hyatt, Rinaldo Rodrigues Dos Passos, Fenix A Araujo, Emily W Wilson, Emily W Waigi, Tiago J Costa, Darízy F Silva, R Clinton Webb, Camilla F Wenceslau, Cameron G McCarthy","doi":"10.1111/micc.70063","DOIUrl":"10.1111/micc.70063","url":null,"abstract":"<p><strong>Objective: </strong>Perivascular adipose tissue (PVAT) surrounds most peripheral blood vessels and exerts an anti-contractile influence through paracrine mediators. Although numerous vasoactive factors have been identified, the mechanisms linking adipocyte metabolism to PVAT-dependent modulation of vascular tone remain poorly defined. Because adipocytes store energy as triglycerides hydrolyzed by adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) to generate free fatty acids, we hypothesized that lipolysis-derived fatty acids may contribute to PVAT's anti-contractile actions through activation of long-chain fatty acid-sensing G protein-coupled receptors, Gpr40 and/or Gpr120.</p><p><strong>Methods: </strong>Mesenteric resistance arteries (MRAs) from adult Wistar rats were studied using wire myography, with or without PVAT, and pharmacological agonists/antagonists and endothelial denudation were used to study signaling. To examine changes in hypertension, PVAT and MRAs from spontaneously hypertensive rats (SHRs) were analyzed by western blotting, and plasma from non-fasting or fasting SHR was assessed by untargeted lipidomics.</p><p><strong>Results: </strong>In Wistar rats, inhibition of ATGL, but not HSL, abolished PVAT's anti-contractile effect, and blockade of Gpr40, but not Gpr120, similarly diminished this response, identifying ATGL and Gpr40 as important mediators. Activation of Gpr40 in PVAT- and endothelium-denuded MRAs further recapitulated the anti-contractile effect in a β-arrestin-dependent manner. In SHR, PVAT ATGL expression was significantly upregulated and MRA Gpr40 expression tended to increase. However, circulating Gpr40 ligand abundance was largely unchanged between strains, suggesting that impaired ligand availability is unlikely to underlie PVAT dysfunction in hypertension.</p><p><strong>Conclusions: </strong>These findings identify a previously unrecognized ATGL-Gpr40 signaling axis linking adipocyte triglyceride metabolism to PVAT-mediated regulation of vascular tone.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 4","pages":"e70063"},"PeriodicalIF":2.4,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13136784/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147817160","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":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148091644","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":"Correction to “MiR-98-5p Promotes Ischemia/Reperfusion-Induced Microvascular Dysfunction by Targeting NGF and Is a Potential Biomarker for Microvascular Reperfusion”","authors":"","doi":"10.1111/micc.70057","DOIUrl":"10.1111/micc.70057","url":null,"abstract":"<p>Hu, Y., J. Xiong, H. Wen, H. Wei, and X. Zeng. 2021. “MiR-98-5p Promotes Ischemia/Reperfusion-Induced Microvascular Dysfunction by Targeting NGF and Is a Potential Biomarker for Microvascular Reperfusion.” <i>Microcirculation</i> 28: e12657. https://doi.org/10.1111/micc.12657.</p><p>We noticed that the three representative H&amp;E images in Figure 4B contain partial overlap, involving the I/R group and the I/R + antagomiR-vector group in Figure 4B, as well as the I/R + antagomiR-98-5p group. In addition, the representative gelatin–ink perfusion images in Figure 4C for the I/R + antagomiR-98-5p group and the I/R + CPZ + antagomiR-98-5p group also appear to partially overlap.</p><p>We believe this resulted from an error during figure assembly due to inadequate organization of our original image archive, which led to incorrect selection of representative panels.</p><p>To correct the published record and ensure transparency, we have re-selected the correct representative images from the original experiments and prepared revised panels for Figures 4B and 4C.</p><p>In addition, upon re-checking the manuscript, we noticed that the published Western blot image (Figure 7A) is not optimal for presentation. Specifically, the background appears overexposed and the image contains pronounced noise/speckling and scratch- or streak-like scanning artifacts, which reduce band-to-background contrast and may hinder accurate visual assessment of the NGF signal. To avoid any potential confusion, we propose to replace Figure 7A with a clearer representative image.</p><p>We apologize for this error.</p>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639363","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":"Tau Oligomers Induce Brain Endothelial Cell Hyperpermeability and Increase NLRP3 Inflammasome Signaling and MMP-9 Activity.","authors":"Gabriela Seplovich, Saravanakumar Muthusamy, Aliyah Anderson, O'lisa Yaa Waithe, Firas Kobeissy, Kevin K Wang, Binu Tharakan","doi":"10.1111/micc.70059","DOIUrl":"10.1111/micc.70059","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;Microvascular hyperpermeability and blood-brain barrier (BBB) dysfunction is a key consideration in neurological disorders, particularly tauopathies, a group of neurodegenerative disorders driven by misfolded and aggregated tau protein. Tau pathology has been shown to activate microglial NLRP3 inflammasome, an innate immune system sensor that responds to changes in the microenvironment, including cellular stress. Increases in reactive oxygen species (ROS), for example, activate NLRP3 inflammasome signaling, which provides a platform for the maturation of caspase-1 enzyme. Mature caspase-1 can cleave and release pro-inflammatory IL-1β cytokine. Both NLRP3 inflammasome and IL-1β may activate downstream MMP-9 enzyme, a known inducer of endothelial cell barrier hyperpermeability. Endothelial cells make up the innermost layer of the BBB and as such, largely govern BBB structural and functional integrity. Whether tau can activate NLRP3 inflammasome signaling in cerebral endothelial cells is unknown. The objective of this study is therefore to understand the role of tau, in various states of aggregation, on endothelial cell permeability and to investigate if NLRP3 inflammasome signaling occurs in this context.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Human brain microvascular endothelial cells (HBMECs) were grown as a monolayer in Transwell inserts and exposed to various tau polymorphs, including tau monomers, tau oligomers (oTau), and tau fibrils (fTau). Barrier permeability was measured using FITC-dextran fluorescent tracer (10 kDa) and Trans-Endothelial Electrical Resistance (TEER). Relative changes in gene expression were measured using RT-qPCR and normalized to GAPDH. Levels of NLRP3 sensor protein and IL-1β were measured by ELISA. Relative activity of caspase-1 and MMP-9 enzymes was calculated using fluorometry. Cell viability was reported using calcein AM, a measure of cell membrane integrity, and by measuring the redox potential of XTT. ROS formation, apoptosis, and necrosis were determined using commercially available kits. An NLRP3 inflammasome inhibitor, MCC950, was applied in blocking studies prior to tau treatments.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Tau oligomers, but not monomers or fibrils, induced endothelial cell hyperpermeability in a dose-independent manner. At concentrations that compromised barrier function (100 nM; overnight), oTau did not alter cell viability and did not increase apoptosis or necrosis. Tau oligomers increased the formation of ROS and increased levels of both NLRP3 sensor protein and IL-1β cytokine. Enzymatic activity of caspase-1 and MMP-9 also increased in response to oTau, without changes in gene expression. These alterations were attenuated when NLRP3 inflammasome signaling was inhibited via MCC950, strongly suggesting that oTau activates NLRP3 inflammasome signaling in cerebral endothelial cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Our study is the first to document a role for NLRP3 inflamm","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 3","pages":"e70059"},"PeriodicalIF":2.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13420001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775650","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":"Temporal Progression of Microvascular Alterations in the Nailfold and Skeletal Muscle of Non-Obese Type 2 Diabetic Rats","authors":"Miho Kanazashi,&nbsp;Masayuki Tanaka,&nbsp;Toshiko Tsumori","doi":"10.1111/micc.70054","DOIUrl":"10.1111/micc.70054","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Diabetes is associated with microvascular complications in multiple tissues. Nailfold capillaries (NFCs) provide a noninvasive window for assessing microvascular alterations; however, their temporal association with skeletal muscle microvascular changes during diabetes progression remains unclear. This study aimed to determine whether NFC structural changes reflect skeletal muscle microvascular alterations and muscle-type-specific vulnerability in a non-obese type 2 diabetes model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Spontaneously Diabetic Torii (SDT) rats, a non-obese type 2 diabetes model, and age-matched Sprague–Dawley rats were studied. NFC morphology was evaluated by capillaroscopy at 12, 18, and 28 weeks of age. Soleus and plantaris muscles were collected for histological and gene expression analyses, and glucose tolerance was evaluated by oral glucose tolerance testing at each time point.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>At 12 weeks of age, SDT rats exhibited mild glucose intolerance without significant abnormalities in NFC morphology or skeletal muscle capillary indices. At 18 weeks, when glucose intolerance became evident in the absence of persistent hyperglycemia, NFC narrowing and reduced density were observed, accompanied by capillary rarefaction in the predominantly fast-twitch plantaris muscle, whereas the slow-twitch soleus muscle remained relatively preserved. By 28 weeks, persistent hyperglycemia was present, and overt muscle atrophy was observed exclusively in the plantaris muscle.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>NFC structural alterations emerge alongside skeletal muscle microvascular rarefaction at the stage of glucose intolerance and precede overt muscle atrophy in fast-twitch muscle. NFC assessment may serve as a noninvasive indicator of early microvascular alterations relevant to diabetes-associated skeletal muscle deterioration.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444254","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":"Choroidal Microcirculatory Responses to Hemodialysis in Patients With Diabetic Nephropathy and Retinopathy","authors":"Ryuya Hashimoto,&nbsp;Kazufumi Tanaka,&nbsp;Naoki Fujioka,&nbsp;Moe Nunose,&nbsp;Sara Imai,&nbsp;Serika Moriyama,&nbsp;Mai Hitaka,&nbsp;Keisuke Yamazaki,&nbsp;Fumihiko Yagi,&nbsp;Yasushi Ohashi","doi":"10.1111/micc.70055","DOIUrl":"10.1111/micc.70055","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To investigate choroidal hemodynamic changes after a hemodialysis (HD) session in the initiation versus maintenance phases in patients with diabetic nephropathy (DN) and diabetic retinopathy (DR).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study included 38 eyes of 20 patients with DN-related end-stage renal disease and DR, stratified into initiation (first HD session; 12 eyes) and maintenance (26 eyes) groups. Choroidal hemodynamics were quantified using laser speckle flowgraphy (LSFG). Macular mean blur rate (M_MBR; index of blood flow) parameters, macular beat strength (M_BS; index of pulsatility), and central choroidal thickness (CCT) were evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In the initiation group, M_MBR parameters significantly decreased after HD, whereas mean changes in M_BS and CCT were not significant. A comparable significant reduction in ocular perfusion pressure was observed in both cohorts. The initiation group exhibited significantly greater reductions in choroidal circulation and thickness. Higher ultrafiltration volume was linked to greater flow pulsatility reductions in the initiation group, with no volume-dependent correlation in the maintenance group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Choroidal circulation exhibits dialysis phase-dependent hemodynamic patterns. The initiation phase is characterized by volume-dependent flow pulsatility reductions, whereas the maintenance phase displays an attenuated response, indicating vascular adaptation. LSFG-derived monitoring may serve as a noninvasive biomarker for assessing microcirculatory responses.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147434206","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":"Protective Effects of Pentoxifylline on Peripheral Microcirculatory Dysfunction and Renal Cortical Oxygen Deficiency in a Rat Model of LPS-Induced Sepsis","authors":"Bülent Ergin,&nbsp;H. Rob Taal,&nbsp;Deniz Erol Kutucu,&nbsp;Wijnie van Dam,&nbsp;Aysegul Kapucu,&nbsp;Sinno S. H. P. Simons,&nbsp;Can Ince,&nbsp;Irwin K. M. Reiss","doi":"10.1111/micc.70056","DOIUrl":"10.1111/micc.70056","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Sepsis is associated with hypotension, tissue hypoperfusion, and microcirculatory dysfunction leading to multi-organ failure and mortality. Pentoxifylline (PTX), a phosphodiesterase inhibitor, is reported to improve blood flow and viscosity. The aim of this study was to investigate the efficacy of PTX on peripheral and renal microcirculatory alterations in sepsis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Fully instrumented Wistar albino rats were randomized as the control group (only surgery), only lipopolysaccharide (LPS) group without treatment (T1), LPS group with PTX treatment (LPS + PTX), LPS group treated with only fluid resuscitation (Ringer's acetate; RA), LPS + RA, LPS group with combined treatment with PTX and RA (LPS + PTX + RA) for 3 h (T2, T3 and T4). The systemic hemodynamics, renal oxygenation, leg muscle microcirculation, histological damage, and inflammatory and endothelial injury markers were analyzed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The renal cortical microvascular oxygen pressure (cμPO₂) was improved by the PTX, RA, and PTX + RA treatments compared to the LPS group (<i>p</i> &lt; 0.05). The proportions of perfused vessels (PPV) and red blood cell velocity (RBCv) were significantly restored by PTX and RA compared with the LPS group at T4 (<i>p</i> &lt; 0.05). Renal damage and inflammatory cell infiltration were reduced by PTX and RA together compared with RA alone (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In this study, we found that PTX may protect renal oxygenation, peripheral (muscle) microcirculation, renal damage, and tissue inflammatory cell infiltration in a rat model of LPS-induced sepsis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147390639","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":"Abstracts From the 50th Annual Meeting of Japanese Society for Microcirculation","authors":"","doi":"10.1111/micc.70053","DOIUrl":"10.1111/micc.70053","url":null,"abstract":"","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"33 2","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147284449","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}