Acta Physiologica最新文献

{"title":"Cardiomyocyte-Specific Deletion of Sirtuin 5 Accelerates the Development of Heart Failure Upon Dysregulating Purine Metabolism","authors":"Nikole J. Byrne,&nbsp;Christoph Koentges,&nbsp;Katharina Pfeil,&nbsp;Julia C. Lueg,&nbsp;Sayan Bakshi,&nbsp;Aleksandre Tarkhnishvili,&nbsp;Ivan Vosko,&nbsp;Johannes Gollmer,&nbsp;Laura C. Birkle,&nbsp;Thomas Rathner,&nbsp;Stephan Birkle,&nbsp;Sibai Tang,&nbsp;Clara Rau,&nbsp;Michael M. Hoffmann,&nbsp;Katja E. Odening,&nbsp;Stephen Barnes,&nbsp;Landon Shay Wilson,&nbsp;Senka Ljubojevic-Holzer,&nbsp;Markus Wallner,&nbsp;Dirk von Lewinski,&nbsp;Peter Rainer,&nbsp;Simon Sedej,&nbsp;Harald Sourij,&nbsp;Christoph Bode,&nbsp;Adam R. Wende,&nbsp;Andreas Zirlik,&nbsp;Heiko Bugger","doi":"10.1111/apha.70120","DOIUrl":"10.1111/apha.70120","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Sirtuin 5 (SIRT5), a mitochondrial NAD⁺-dependent deacylase, regulates fundamental cellular pathways, including energy substrate metabolism. The current study is designed to better elucidate the role of SIRT5 in the development of heart failure (HF).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Mice with cardiomyocyte-specific deletion (<i>cSirt5</i>^−/−) or overexpression (c<i>Sirt5</i>-Tg) of SIRT5 were generated and subjected to chronic pressure overload by transverse aortic constriction (TAC) or Sham surgery. Cardiac structure and function were assessed by echocardiography, isolated heart perfusions, and histology. MS-based metabolomics and bulk RNA sequencing were used to explore metabolic and molecular signatures.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>c<i>Sirt5</i>-Tg mice had similar cardiac structure and function compared to control mice, whereas c<i>Sirt5</i>^−/− mice displayed exacerbated cardiac dilation and dysfunction following TAC, measured both in vivo by echocardiography and ex vivo in isolated heart perfusions. Metabolomics revealed accumulation of inosine and hypoxanthine, and depletion of adenosine, adenine, AMP, and ADP in c<i>Sirt5</i>^−/− hearts and following TAC, indicating dysregulation of purine metabolism. RNA-sequencing uncovered upregulation of purine-nucleoside phosphorylase and 5′ nucleotidase, and downregulation of adenosine kinase (ADK) in c<i>Sirt5</i>^−/− hearts following TAC, indicating dysregulation at the interface of adenosine nucleotide salvage and purine degradation in the absence of SIRT5. Analyses of left ventricular tissue of patients with HF revealed reduced SIRT5 expression correlating with reduced ADK expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Loss of SIRT5 in cardiomyocytes aggravates cardiac remodeling and dysfunction in response to chronic pressure overload, involving ATP precursor depletion due to transcriptional dysregulation of cardiac purine metabolism.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70120","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145306344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fentanyl Disrupts Vagal Control of Airway Tone to Induce Transient Obstruction","authors":"Riley R. Parks,&nbsp;Marissa J. Andersen,&nbsp;Mackenna L. Hatfield,&nbsp;Nicholas J. Burgraff","doi":"10.1111/apha.70119","DOIUrl":"10.1111/apha.70119","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Opioid-induced respiratory depression (OIRD) is the primary cause of death in opioid overdose, resulting from both suppressed respiratory rhythm and increased airway and thoracic rigidity that compromise ventilation and resuscitation. While the effect(s) of opioids on central rhythm-generating circuits are well documented, the mechanisms leading to airway obstruction remain poorly understood. Here, we investigated the hypothesis that enhanced vagal parasympathetic output contributes to fentanyl-induced airway disruption.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In urethane-anesthetized mice, diaphragm electromyography (EMG), respiratory airflow, and vagus nerve activity were recorded in-vivo before and after intraperitoneal fentanyl administration (500 μg/kg). The effects of bilateral vagotomy, atropine administration, and intracisternal naloxone were evaluated to determine the contribution of vagal pathways and central opioid receptor mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Fentanyl caused a characteristic slowing of respiratory rate accompanied by a compensatory increase in tidal volume, but also produced a transient delay between diaphragm activation and airflow onset, consistent with airway obstruction. This delay was abolished by bilateral vagotomy or atropine and reversed by intracisternal naloxone, implicating central vagal mechanisms. Vagal electroneurograms showed increased tonic multiunit activity and enhanced large-amplitude single-unit firing, particularly within efferent fibers, together with a loss of normal inspiratory phase-locking. The magnitude of tonic vagal activation strongly correlated with the severity of airway disruption.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Fentanyl disrupts respiratory-autonomic integration by enhancing parasympathetic vagal drive, producing a central, opioid receptor-mediated mechanism of airway constriction. Targeting vagal pathways may therefore represent a promising adjunctive strategy for improving airway patency and ventilatory recovery during opioid overdose reversal.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12522075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145290389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary Nitrate Prevents Cardiac Dysfunction in HFrEF by Improving Hemodynamics, Ameliorating Remodeling, and Resolving Inflammation","authors":"Miho Shimari,&nbsp;Gaia Picozzi,&nbsp;Ariela Boeder,&nbsp;Drielle Dantas Guimarães,&nbsp;Zhengbing Zhuge,&nbsp;Jon O. Lundberg,&nbsp;Mattias Carlstrom,&nbsp;Lars H. Lund,&nbsp;Daniel C. Andersson,&nbsp;Gianluigi Pironti","doi":"10.1111/apha.70115","DOIUrl":"10.1111/apha.70115","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Impaired cardiac function, reduced nitric oxide (NO) bioavailability, and inflammation are key contributors to the pathogenesis and progression of heart failure with reduced ejection fraction (HFrEF). This study aimed to investigate whether dietary inorganic nitrate supplementation can attenuate cardiac dysfunction and adverse remodeling in HFrEF by enhancing NO signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Two mouse models of HFrEF, induced by myocardial infarction (MI) or transverse aortic constriction (TAC), were treated with dietary nitrate or a control diet for 4–6 weeks, initiating the treatment on day 3 after myocardial injury. Echocardiography and pressure volume (PV) loop analysis were employed to assess cardiac function and hemodynamics. Histology staining was performed to assess the degree of cardiac fibrosis. Myograph experiments were conducted to assess aortic vasorelaxation. Biomarkers related to hypertrophy, fibrosis, and inflammation were analyzed in cardiac tissues through Q-PCR analysis and immunofluorescence staining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In HFrEF mice, long-term inorganic nitrate treatment increased systolic and diastolic function, enhanced vascular relaxation, and reduced both replacement and reactive fibrosis. In the nitrate group, cardiac gene expression showed downregulation of hypertrophy-, fibrosis-, and inflammation-related markers, alongside upregulation of anti-inflammatory markers associated with M1-to-M2 macrophage polarization. Immunofluorescence confirmed reduced fibrosis and increased anti-inflammatory protein biomarkers associated with increased serum nitrate and cardiac cGMP levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Early initiation of dietary nitrate supplementation after myocardial injury enhances cardiac and vascular function, reduces fibrosis and inflammation, and holds promise as a cardioprotective strategy to reduce the progression of HFrEF through NO-signaling.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12516936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145278470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transduction Mechanisms for Cold Temperature in Mouse Trigeminal and Vagal Ganglion Neurons Innervating Different Peripheral Organs","authors":"Katharina Gers-Barlag,&nbsp;Ana Gómez del Campo,&nbsp;Pablo Hernández-Ortego,&nbsp;Eva Quintero,&nbsp;Félix Viana","doi":"10.1111/apha.70111","DOIUrl":"10.1111/apha.70111","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To elucidate the molecular mechanism of cold sensing by visceral sensory endings, a side-by-side characterization of cold-sensitive (CS) neurons in adult mouse trigeminal (TG) and vagal ganglia (VG) was performed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A combination of physiological, pharmacological, molecular, and genetic tools was employed on trigeminal and vagal neurons.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CS neurons are more abundant in VG, and the majority co-express TRPA1. Cold-evoked responses are severely blunted in <i>Trpa1</i> KO mice. In contrast, TRPM8 deletion or pharmacological TRPM8 blockade had little impact on VG cold sensitivity. In <i>Trpm8</i>^<i>eYFP</i> reporter mice, VG TRPM8 expression was restricted to the rostral jugular ganglion. In vivo labeling of airway-innervating VG neurons demonstrated their enhanced cold sensitivity and higher TRPA1 expression compared to neurons innervating the stomach wall. In contrast, the majority of CS TG neurons co-express TRPM8 markers, and their cold sensitivity is reduced after TRPM8 deletion or blockade. However, pharmacological or genetic ablation of TRPA1 confirmed its contribution to high-threshold cold sensitivity in TG, suggestive of a role in noxious cold sensing. In both ganglia, a fraction of CS neurons responded to cooling by a mechanism independent of TRPA1 or TRPM8. Blocking potassium channels enhanced cold sensitivity independently of the specific transducer mechanism, suggestive of a common excitability brake mechanism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The study highlights the differential contribution of TRPM8 and TRPA1 channels to cold sensitivity in somatic and visceral ganglia, establishing a critical role of TRPA1 channels in visceral cold transduction. Finally, cold sensitivity seems fine-tuned to the specific physiological needs of different organs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70111","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of Preeclampsia and Gestational Diabetes on Future Maternal Cardiometabolic Health","authors":"Alice M. Barrell,&nbsp;Amanda N. Sferruzzi-Perri","doi":"10.1111/apha.70113","DOIUrl":"10.1111/apha.70113","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Pregnancy is a time of significant maternal physiological change to meet the metabolic demands of the feto-placental unit. In cases of pregnancy complications, mal-adaptive physiological responses may occur, potentially impacting the health of both mother and fetus. Moreover, some maternal changes may persist beyond delivery. Although the clinical symptoms of preeclampsia (PE) and gestational diabetes mellitus (GDM) usually resolve post-partum, growing evidence suggests that these conditions confer a lifelong increased risk of cardiometabolic disease in affected women. This review aimed to summarize epidemiological evidence linking PE and GDM to future maternal cardiometabolic disorders, explore potential underlying mechanisms based on animal and small-scale human studies, and discuss implications for future research and postpartum clinical care.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Targeted PubMed searches were conducted to search for relevant publications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Data suggest that pregnancy complications may both reveal an underlying predisposition to cardiometabolic disease and induce lasting physiological changes that contribute to future health risks. Notably, women with a history of PE may have a 3–4-fold increased risk of cardiovascular disease, while those with prior GDM may face up to a 10-fold higher risk of developing type 2 diabetes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Pregnancy offers a valuable window into a woman's future health, presenting a unique opportunity for preventative medicine for up to half of the world's population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal Differences of GABAergic Polarization and Shunting During Dendritic Integration","authors":"Yulia Dembitskaya,&nbsp;Artem Kirsanov,&nbsp;Yu-Wei Wu,&nbsp;Alexey Brazhe,&nbsp;Alexey Semyanov","doi":"10.1111/apha.70112","DOIUrl":"https://doi.org/10.1111/apha.70112","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>In the adult brain, GABA exerts either depolarizing or hyperpolarizing effects on neuronal membranes, depending on neuron type, subcellular location, and neuronal activity. Depolarizing GABA typically inhibits neurons through shunting, which is mediated by increased membrane conductance upon GABA_A receptor activation; however, it can also excite neurons by recruiting voltage-dependent conductances. The net influence of these opposing actions of depolarizing GABA on glutamatergic synaptic inputs remains incompletely understood. We aimed to examine the spatiotemporal characteristics of membrane polarization and shunting mediated by GABA_A receptors and assess their functional impact on the integration of GABAergic and glutamatergic inputs along dendrites.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using whole-cell current-clamp recordings in CA1 pyramidal neurons and dentate gyrus granule cells (GCs) from rat hippocampal slices, we mimicked GABAergic and glutamatergic inputs with local GABA puff and glutamate spot-uncaging, respectively. A mathematical model further quantified the relative effects of local shunting and polarization.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Depolarizing GABAergic postsynaptic responses (GPSRs) exhibited biphasic actions, exerting inhibitory effects at the synapse through shunting, and excitatory effects distally, where depolarization predominated. The excitatory component also persisted longer than the shunting inhibition. In contrast, hyperpolarizing GPSRs remained consistently inhibitory across both spatial and temporal dimensions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These findings highlight the complex spatiotemporal interplay between shunting and membrane polarization mediated by GABAergic inputs, providing new insights into dendritic computation and neuronal network dynamics.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 11","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Being a Biomarker: Lipocalin-2/NGAL as a Facilitator for Protective Drug Action in Hypoxic Kidney Injury","authors":"Boye L. Jensen","doi":"10.1111/apha.70110","DOIUrl":"10.1111/apha.70110","url":null,"abstract":"&lt;p&gt;In the present issue of &lt;i&gt;Acta Physiologica&lt;/i&gt; [&lt;span&gt;1&lt;/span&gt;], an international consortium of investigators reports that the iron-transporter glycoprotein lipocalin-2 (LCN2), originally identified in neutrophils and named &lt;i&gt;neutrophil gelatinase-associated lipocalin&lt;/i&gt;, abbreviated NGAL or 24p3, may protect the kidneys from ischemia–reperfusion injury. The findings suggest that LCN2 protects the kidneys by restoring the sensitivity of soluble guanylate cyclase (sGC) to drug activators in afferent glomerular arterioles through a receptor-mediated mechanism. LCN2 is produced and released by several tissues including adipose tissue, liver, kidneys, and neutrophils. It is categorized as an acute-phase protein that is upregulated during inflammatory states. LCN2 is widely used in clinical and experimental settings as an early biomarker in acute kidney injury and for the staging of chronic kidney disease.&lt;/p&gt;&lt;p&gt;The study by Zhao et al. [&lt;span&gt;1&lt;/span&gt;] is an elegant follow-up study on a series of independent observations dating 10–20 years back, which include a study by authors from 2016 [&lt;span&gt;2&lt;/span&gt;]. A consistent kidney-protective effect of exogenous LCN2 was found in preclinical kidney ischemia-injury models, including a kidney transplantation model. The study in &lt;i&gt;Acta&lt;/i&gt; shows ex vivo with murine, isolated kidney microvessels, that LCN2 mitigates excessive microvascular resistance through restoring vascular smooth sGC sensitivity towards activator drugs. The sensitivity is typically lost by more severe prolonged hypoxia. Soluble GCs can be oxidized to the heme-free form, apo-sGC, and the authors confirm that apo-sGC cannot be activated by the endogenous agonist nitric oxide (NO). The class of sGC activator drugs is unique and different from sGC stimulators since they can overcome this state and activate apo-sGC independently of NO to increase target cell cyclic guanosine monophosphate (cGMP) production even under detrimental oxidative stress. Zhao et al. [&lt;span&gt;1&lt;/span&gt;] show that LCN2 restores sensitivity of the kidney afferent arterioles towards sGC activators dependent on iron. The effect is found in arterioles subjected to hypoxia ex vivo after isolation and in arterioles subjected to hypoxia “in situ” in transplanted kidneys before microdissection and testing. The conclusion is that by delivering ferric iron bound to LCN2 (holo-LCN2) to arterioles, this oxidizes sGC, which restores sensitivity to activator drugs. The study corroborates that LCN2 may be a direct, extracellular, signaling molecule that indirectly protects vascular smooth muscle suffering from prolonged ischemic insults in the kidneys (Figure 1).&lt;/p&gt;&lt;p&gt;What is the mechanism? LCN2 binds hydrophobic microbial siderophores, which are small molecules that bacteria produce to sequester iron from their environment. The acute phase reactant LCN2 is thereby bacteriostatic since iron is a vital nutrient for many microbes. Deletion of LCN2 increases susceptibility to &lt;i&gt;Esch","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 10","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145123858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Micro-Embolic Events and Their Clearing in the Brain. A Narrative Review","authors":"Kevin Mol,&nbsp;Inge A. Mulder,&nbsp;Ed van Bavel","doi":"10.1111/apha.70098","DOIUrl":"https://doi.org/10.1111/apha.70098","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The cerebral circulation is continuously challenged by intravascular micrometer-sized particles that become trapped microvascular-emboli. These particles may include micro-thrombi, stiffened erythrocytes, and leukocytes, while also fat particles, air, and microplastics may cause microvascular embolism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Review Scope</h3>\u0000 \u0000 <p>In this narrative review, we discuss these embolization processes and their acute and chronic consequences. These relate to the local flow interruption as well as the direct interaction with the endothelium. In addition, we address the clearing processes, including local thrombolysis and extravasation, or angiophagy, of the emboli.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>A continuous balance exists between embolic events and their resolution under normal conditions. Increased micro-embolic rates, as occur in e.g., atrial fibrillation, or decreased clearing, possibly related to endothelial cell dysfunction, disturb this balance. This could lead to continuing loss of capillaries, micro-infarcts, and cognitive decline.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 10","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145021990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poster Session B","authors":"","doi":"10.1111/apha.70105","DOIUrl":"https://doi.org/10.1111/apha.70105","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 S735","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145012239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Symposia","authors":"","doi":"10.1111/apha.70101","DOIUrl":"https://doi.org/10.1111/apha.70101","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 S735","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145012241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}