Microvascular research最新文献

{"title":"Sex differences in near-infrared spectroscopy reactive hyperemia: Influence of adipose tissue and desaturation rate","authors":"Matthew A. Chatlaong ,&nbsp;Hannah C. Dowell ,&nbsp;Orlandria J. Smith ,&nbsp;Matthew B. Jessee","doi":"10.1016/j.mvr.2025.104865","DOIUrl":"10.1016/j.mvr.2025.104865","url":null,"abstract":"<div><div>Sex differences in near-infrared spectroscopy (NIRS) reactive hyperemia outcomes have been previously reported, with females generally having a lower reperfusion slope. Sex differences have also been reported for adipose tissue thickness (ATT), which affects the NIRS signal, and desaturation during occlusion, which may act on reperfusion slopes. We aimed to compare statistically adjusted and unadjusted sex differences in reperfusion slope during reactive hyperemia.</div></div><div><h3>Methods</h3><div>23 female and 22 male participants completed forearm and thigh vascular occlusion tests. ATT was measured via ultrasound. Reperfusion slopes (StO₂%/s) were compared between sexes using linear models with and without desaturation slope (StO₂%/s) and ATT as covariates. Results are mean or mean difference [95 % CI].</div></div><div><h3>Results</h3><div>In both limbs, females had greater ATT (<em>p</em> &lt; 0.001). Desaturation rate was lower in females for the leg (−0.02 [−0.03, −0.01]), but not the arm (0.00 [−0.01, 0.02]). Unadjusted, males had greater reperfusion slope in the leg (females = 0.91 [0.70, 1.11], males = 1.59 [1.33, 1.85], <em>p</em> &lt; 0.001) but not the arm (females = 1.60 [1.36, 1.84], males = 1.57 [1.29, 1.86], <em>p</em> = 0.874). Sex differences were not observed in adjusted models (both <em>p</em> ≥ 0.631). ATT and desaturation slope explained unique variance in the leg (both <em>p</em> ≤ 0.001), but only desaturation slope did in the arm (<em>p</em> &lt; 0.001).</div></div><div><h3>Conclusion</h3><div>Sex differences may have been related to differing ATT and desaturation rates. Researchers may consider adjusting for ATT and/or desaturation rate when estimating sex differences with NIRS reactive hyperemia.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104865"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030165","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":"Clinical profile and long-term outcomes of chest pain patients with coronary microvascular dysfunction from the emergency department – results from the Yale-CMD registry","authors":"Basmah Safdar ,&nbsp;Bin Zhou ,&nbsp;Fangyong Li ,&nbsp;Paolo G. Camici ,&nbsp;James Dziura ,&nbsp;Ania M. Jastreboff ,&nbsp;Alexandra Lansky ,&nbsp;Samit M. Shah ,&nbsp;Albert Sinusas ,&nbsp;Erica Spatz ,&nbsp;Gail D'Onofrio","doi":"10.1016/j.mvr.2025.104878","DOIUrl":"10.1016/j.mvr.2025.104878","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the long-term prognosis of coronary microvascular dysfunction (CMD) in emergency department (ED) patients with chest pain for major adverse cardiac events (MACE) due to all-cause mortality, myocardial infarction (MI), heart failure (HF), or stroke.</div></div><div><h3>Methods</h3><div>A prospective cohort of ED patients evaluated by hybrid cardiac positron emission tomography with attenuation computed tomography within 24 h of arrival. Patients were classified as: (1) Controls – coronary flow reserve (CFR) ≥2 without perfusion defect or coronary calcification; (2) CMD: CFR &lt;2 without defect or calcification; or (3) CAD/CALC – established or new coronary artery disease (CAD) or calcification (CALC). We conducted annual follow-ups for MACE and all-cause healthcare utilization (hospitalizations and ED visits). We adjusted incidence rates (aIR) and hazard ratio (aHR) for demographics, comorbidities, and medications.</div></div><div><h3>Results</h3><div>Between 2014 and 2020, 189 patients were enrolled: 95 (50 %) Controls, 34 (18 %) with CMD, and 60 (32 %) with CAD/CALC. Median follow-up time was 50 months (38–92), and a total of 187 unique MACE were recorded in 44 patients. CMD patients had 4× higher MACE risk than controls (aIR 3.8; 95 % CI: 2.1–6.6). CAD/CALC patients had similarly higher risk than controls (aIR: 4.5; 95 % CI: 2.6–7.8). CMD patients had 4× higher risk for time to first MACE than controls (aHR: 3.6; 95 % CI: 1.2–10.7) and higher healthcare utilization per 100 person-months (aIR: 124; 95 % CI: 119–130). Using Seattle Angina Questionnaire, CMD patients showed worse angina frequency than controls (difference: -16.4, 95 % CI: −29.5 to −3.4).</div></div><div><h3>Conclusions</h3><div>Patients with contemporary phenotypes of ischemia (CMD and CAD/CALC) had higher adverse events than controls, positing ED encounters as an opportunity for early identification and treatment.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104878"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145329555","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":"DOT1L-mediated H3K79me1 transcriptional activation of Acp5 aggravates inflammatory responses following diabetic vascular injury","authors":"Jing Zhang ,&nbsp;Zishu Yang ,&nbsp;Li Liu ,&nbsp;Di Wu ,&nbsp;Chen Cheng ,&nbsp;Peng Zhu ,&nbsp;Wei Wang ,&nbsp;Wenqiang Li ,&nbsp;Hua Deng ,&nbsp;Yudiyang Ma ,&nbsp;Cuiyuan Huang ,&nbsp;Jian Yang","doi":"10.1016/j.mvr.2025.104882","DOIUrl":"10.1016/j.mvr.2025.104882","url":null,"abstract":"<div><h3>Background</h3><div>Hyperinsulinemia-induced inflammatory responses are a key pathological basis for diabetic proliferative vascular lesions. However, DOT1L impact on vascular repair following diabetic injury and the underlying mechanism remain unclear.</div></div><div><h3>Methods</h3><div>Recombinant lentiviral vectors were constructed to target the upregulation or downregulation of DOT1L expression. Carotid artery balloon injury (BI) model was established in diabetic rats. In vitro experiments, an insulin (INS)-stimulated vascular smooth muscle cell (VSMC) model was used. Inflammatory factor levels, vascular intimal hyperplasia and hemodynamics, H3K79me enrichment in promoter regions were detected. ChIP-Seq was used to evaluate the distribution of proteins and genes, and the levels of proteins implicated in related pathways were analyzed.</div></div><div><h3>Results</h3><div>We found that both in diabetic rat carotid artery tissues 28 days post-BI and in VSMCs after 12 h of insulin stimulation, DOT1L, H3K79me1, IL-6 and TNF-α levels were markedly increased. Overexpression of DOT1L enhanced the expression and release of IL-6 and TNF-α in insulin-induced VSMCs, increased the enrichment of H3K79me1 at the Acp5 gene promoter by 3.92-fold, promoted ACP5 expression, inhibited β-catenin phosphorylation, and upregulated NLRP3 levels. Conversely, downregulation of DOT1L had the opposite effects. In arteries overexpressing DOT1L, inflammatory factor expression and release were markedly enhanced, accompanied by triggering of the ACP5/β-catenin/NLRP3 signaling pathway, roughened intimal surfaces, reduced lumen diameters, decreased residual blood flow area, and increased diameter stenosis rate; greater intimal thickness, and a higher intima/media ratio. In contrast, downregulation of DOT1L exhibited opposite effects.</div></div><div><h3>Conclusion</h3><div>DOT1L aggravates the inflammatory response following diabetic vascular injury by transcriptionally activating Acp5 through H3K79me1, inhibiting β-catenin phosphorylation and inactivation, and upregulating NLRP3 expression.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104882"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145445309","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":"Involvement of monocarboxylate transporter 7 in taurine efflux transport from rat retinal pericytes and capillary endothelial cells","authors":"Yuma Tega ,&nbsp;Fuki Kusakabe ,&nbsp;Shin-ichi Akanuma ,&nbsp;Ken-ichi Hosoya","doi":"10.1016/j.mvr.2025.104876","DOIUrl":"10.1016/j.mvr.2025.104876","url":null,"abstract":"<div><h3>Purpose</h3><div>Taurine exists abundantly in the retina and plays a vital role in retinal function. Monocarboxylate transporter 7 (MCT7) is found as a facilitative taurine transporter; however, its involvement in taurine dynamics in the retina is not yet fully understood. The purpose of the present study is to clarify the protein expression and function of MCT7 in retinal cells.</div></div><div><h3>Methods</h3><div>Guinea pig antibodies were raised against the amino acid residues of rat MCT7, and immunostaining was performed to clarify protein expression in the rat retina. To characterize taurine influx into retinal pericytes, a [³H]taurine transport assay was conducted using TR-rPCT1 cells, immortalized rat retinal pericytes. A knockdown assay using MCT7 small interfering RNA (siRNA) was performed to examine the involvement of MCT7 in taurine efflux in TR-rPCT1 and immortalized rat retinal capillary endothelial (TR-iBRB2) cells.</div></div><div><h3>Results</h3><div>The MCT7 protein expression was observed throughout the retinal layer. Immunostaining of isolated retinal capillaries revealed MCT7 expression in retinal pericytes and capillary endothelial cells. [³H]Taurine influx transport in TR-rPCT1 cells depends on temperature, concentration (<em>K</em>_m = 11.2 μM), and extracellular Na⁺ and Cl⁻, and was inhibited by substrates for taurine transporter (TauT), suggesting the involvement of TauT in taurine influx in retinal pericytes. Moreover, MCT7 siRNA decreased MCT7 expression and [³H]taurine efflux in TR-rPCT1 and TR-iBRB2 cells, suggesting that the taurine efflux transport involves MCT7 at least partly.</div></div><div><h3>Conclusions</h3><div>The present study revealed that MCT7 functions as a taurine efflux transporter in both retinal pericytes and capillary endothelial cells.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104876"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102683","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":"Nailfold video capillaroscopy predicts severe progression at three years in systemic sclerosis: Results from SCLEROCAP study","authors":"Carine Boulon ,&nbsp;Iban Larrouture ,&nbsp;Sophie Blaise ,&nbsp;Marion Mangin ,&nbsp;Joëlle Decamps-Le Chevoir ,&nbsp;Patricia Senet ,&nbsp;Isabelle Lazareth ,&nbsp;Nathalie Baudot ,&nbsp;Laurent Tribout ,&nbsp;Bernard Imbert ,&nbsp;François-Xavier Lapébie ,&nbsp;Philippe Lacroix ,&nbsp;Marie-Elise Truchetet ,&nbsp;Julien Seneschal ,&nbsp;Anna Solanilla ,&nbsp;Estibaliz Lazaro ,&nbsp;Isabelle Quéré ,&nbsp;Marc-Antoine Pistorius ,&nbsp;Claire Le Hello ,&nbsp;Edouard Lhomme ,&nbsp;Joël Constans","doi":"10.1016/j.mvr.2025.104874","DOIUrl":"10.1016/j.mvr.2025.104874","url":null,"abstract":"<div><h3>Objectives</h3><div>Systemic sclerosis (SSc) has a variable evolution but may be life-threatening owing to pulmonary, cardiac or renal involvement. Nailfold video capillaroscopy (NVC) is abnormal early in the disease and is crucial for diagnosis. An association between subtypes of scleroderma pattern and disease progression has been suggested. Therefore, we conducted a prospective study to assess whether capillaroscopy can identify SSc patients at risk of progression.</div></div><div><h3>Methods</h3><div>SCLEROCAP was a prospective multicentre observational study that included patients with a diagnosis of SSc followed up for three years. Each patient had yearly standard evaluation and NVC. Images were read by two observers blinded from each other and were classified into subtypes (2 for Maricq's and 3 for Cutolo's classification). Severe progression was defined as cardiac, pulmonary or renal involvement or progression and was assessed by a validation committee.</div></div><div><h3>Results</h3><div>Three hundred and eighty-seven patients were included of whom 369 were followed-up and 53 (14 %) had severe progression. A simple model using Cutolo's capillaroscopic late stage, short duration of disease and age was as powerful in predicting severe progression as a model using all the parameters known to be predictive (AUC[95 %CI] 0.74[0.67–0.82] vs 0.73[0.64–0.77] respectively.</div></div><div><h3>Conclusion</h3><div>NVC is a predictor of severe progression and might be helpful for early therapeutic decisions in patients with SSc.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104874"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086385","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":"Histamine induces vascular endothelial cell proliferation via the histamine H1 receptor–extracellular regulated protein kinase 1/2–cyclin D1/cyclin-dependent kinase 4/6 axis","authors":"Hidenori Wake ,&nbsp;Omer Faruk Hatipoglu ,&nbsp;Takashi Nishinaka ,&nbsp;Masahiro Watanabe ,&nbsp;Takao Toyomura ,&nbsp;Shuji Mori ,&nbsp;Masahiro Nishibori ,&nbsp;Hideo Takahashi","doi":"10.1016/j.mvr.2025.104866","DOIUrl":"10.1016/j.mvr.2025.104866","url":null,"abstract":"<div><div>Histamine is a biogenic amine that plays important roles in the inflammatory phase of physiological wound healing and proliferation of normal and tumor cells. Stimulation of the histamine H1 receptor induces vascular endothelial cell proliferation, possibly contributing to angiogenesis during wound healing and cancer development. However, the specific signaling pathways involved in angiogenesis remain unclear. Based on our previous report that histamine induces endothelial cell tube formation by increasing the vascular endothelial growth factor and matrix metalloproteinase levels via the H1 receptor, we aimed to further examine histamine-induced cell proliferation using EA.hy926 vascular endothelial cells in this study. Histamine phosphorylated extracellular regulated protein kinase-1/2 through the protein kinase C pathway via the H1 receptor and increased c-Fos expression via phosphorylation of Elk-1 and CRE-binding protein. Moreover, c-Fos formed activator protein-1, which further upregulated cyclin D1 expression. Cyclin D1 formed a complex with cyclin-dependent kinase-4/6 and phosphorylated Rb, causing the transcription factor E2F, which is bound to Rb, to dissociate from Rb and induce the factors important for S phase initiation that advance the cell cycle. Overall, our findings in this study to identify H1 receptor-mediated cell proliferation signals in endothelial cells using histamine can aid in the development of new strategies for wound healing and cancer treatment.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104866"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006320","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 association between cutaneous microvascular dysfunction and pulmonary artery hemodynamics in heart transplant candidates","authors":"Antonio Feliciano Fatorelli ,&nbsp;Eduardo Tibirica ,&nbsp;Daniel Arthur Barata Kasal","doi":"10.1016/j.mvr.2025.104877","DOIUrl":"10.1016/j.mvr.2025.104877","url":null,"abstract":"","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104877"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145222030","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":"Retinal neurodegeneration and choroidal changes of early diabetes in peripapillary region detected by swept-source optical coherence tomography angiography","authors":"Zhaoxia Zheng ,&nbsp;Nianen Liu ,&nbsp;Jianing Wang ,&nbsp;Yue Zhang ,&nbsp;Xiaoya Gu ,&nbsp;Shuang Song ,&nbsp;Xiaobing Yu","doi":"10.1016/j.mvr.2025.104867","DOIUrl":"10.1016/j.mvr.2025.104867","url":null,"abstract":"<div><h3>Purpose</h3><div>This study was designed to evaluate peripapillary retinal nerve fiber layer (pRNFL) and choroidal alterations in diabetic patients without diabetic retinopathy (NDR), and further explore their association utilizing ultrawide-field swept-source optical coherence tomography angiography (UWF-SS-OCTA).</div></div><div><h3>Methods</h3><div>This cross-sectional study included 169 eyes of 169 NDR subjects and 54 eyes of 54 healthy controls. pRNFL, choroidal thickness and volume were compared and measured with UWF-SS-OCTA. The association between pRNFL and choroidal parameters was assessed with Spearman correlation analysis. Further multivariate linear regression analysis was performed to evaluate their relationship after adjusting for confounding factors.</div></div><div><h3>Results</h3><div>Compared with healthy controls, NDR patients showed reduced choroidal thickness and volume in the full range and several peripapillary subfields, while a statistical decrease of pRNFL was only detected in the inferior quadrant (<em>P</em> = 0.04). Regarding the distribution profiles in the peripapillary region, the choroid was thickest in the temporal region and thinnest in the inferior region, and a more prominent decrease compared with controls was found in the inferior region. Average pRNFL thickness was independently associated with full-range mean choroidal volume in multiple regression analysis (β = 0.16, <em>P</em> = 0.04).</div></div><div><h3>Conclusion</h3><div>As two early signs of DR, choroidal thinning could precede retinal neurodegeneration. Decreased choroidal thickness may account for the susceptibility of RNFL thinning.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104867"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145048523","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":"Mechanistic investigation of quercetin (an active component of RAS-RH) in modulating radiation-induced coronary microvascular dysfunction via the TCs-ECs crosstalk pathway","authors":"Jiang Hugang ,&nbsp;Liu Ai ,&nbsp;Guo Zeao ,&nbsp;Ren Chunzhen ,&nbsp;Lin Wenyan ,&nbsp;Liu Kai ,&nbsp;Zhao Xinke ,&nbsp;Li Yingdong","doi":"10.1016/j.mvr.2025.104883","DOIUrl":"10.1016/j.mvr.2025.104883","url":null,"abstract":"<div><h3>Background</h3><div>Coronary Microvascular Dysfunction (CMVD), a prevalent comorbidity of various cardiovascular diseases, may contribute to myocardial cell ischemic necrosis. The loss of microvessels—driven by endothelial cells (ECs) apoptosis—is the core pathological hallmarks of CMVD. Our previous studies have established that RAS-RH (<em>Angelica sinensis</em> and <em>Astragalus membranaceus</em> ultrafiltrate) promotes angiogenesis and improves cardiac perfusion. However, its underlying molecular mechanisms remain incompletely understood.</div></div><div><h3>Purpose</h3><div>This study aimed to elucidate the key mechanism by which quercetin, the primary active component of RAS-RH, modulates radiation-induced ECs apoptosis.</div></div><div><h3>Methods</h3><div>Through the integration of network pharmacology and transcriptomics, we identified potential active components of RAS-RH and their key targets involved in regulating the telocytes-endothelial cell (TCs-ECs) crosstalk pathway underlying CMVD. These predictions were further validated using in vitro cellular models via flow cytometry, western blot, wound-healing assays, in situ hybridization, immunofluorescence staining, and EdU proliferation assays.</div></div><div><h3>Results</h3><div>Consistent with our predictions, experimental results demonstrated that quercetin (the primary active component of RAS-RH) significantly upregulated the expression of HIF-1α and miRNA-126 in TCs (<em>P</em> &lt; 0.01) and enhanced miRNA-126 paracrine secretion. Through this paracrine mechanism, quercetin downregulated the expression of Cypd, ANT, F1F0-ATPase, and VDAC in ECs (<em>P</em> &lt; 0.01), inhibited the reduction of mitochondrial membrane potential (ΔΨm) and ECs apoptosis induced by excessive mPTP opening. Collectively, these effects enhanced ECs proliferation, migration, and tube formation capacity, ultimately promoting angiogenesis.</div></div><div><h3>Conclusion</h3><div>These results collectively demonstrate that quercetin, the primary active component of RAS-RH, suppresses excessive mPTP activation and apoptosis while stimulating ECs migration and tube formation. This occurs via upregulating HIF-1α and miRNA-126 expression in TCs and enhancing miRNA-126 paracrine to ECs, positioning the TCs-ECs crosstalk mechanism as a promising novel therapeutic target for intervening in coronary microcirculation dysfunction.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104883"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145471233","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":"Effects of semaglutide on vessel morphology: Studies on the chicken chorioallantoic membrane","authors":"Pei-Hsuan Chen ,&nbsp;Samar Abood ,&nbsp;Steven Bloom","doi":"10.1016/j.mvr.2025.104880","DOIUrl":"10.1016/j.mvr.2025.104880","url":null,"abstract":"<div><div>Glucagon-Like Peptide-1 (GLP-1) receptor agonists are widely used to manage type 2 diabetes and promote weight loss. Semaglutide (SEM)—a long acting GLP-1—has experienced an extraordinary surge in popularity since its approval in 2017. Between 2021 and 2023, SEM prescription fills in the U.S. climbed to 2.56 million <em>per</em> month. Yet, the uptake of SEM into larger populations has raised safety concerns, with provocative findings now suggesting that SEM could negatively affect ocular and reproductive systems, counter to its beneficial effects on the heart. At least some of these concerns involve SEMs ability to alter vascular morphology in these organs. Herein, we study the impact of SEM on vasculature using the well-established chicken chorioallantoic membrane (CAM). This <em>in vivo</em> model mimics vascular beds found in the human eye and placenta and can approximate the effects of drugs on these organs. The CAM also responds to vasoactive drugs in a similar way to the coronary arteries of the heart. Hence, the CAM provides a convenient system to simultaneously interrogate the impact of SEM on ocular, reproductive, and coronary vascular biology. Our studies show that SEM causes vessels to develop with fewer branching points, yielding longer and more direct connections, that shift local blow flow patterns. However, these changes are <em>only</em> significant at SEM concentrations well above the therapeutic dose.</div></div>","PeriodicalId":18534,"journal":{"name":"Microvascular research","volume":"163 ","pages":"Article 104880"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346076","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}