Acta Physiologica最新文献

{"title":"Plenary and keynote abstracts","authors":"","doi":"10.1111/apha.14041","DOIUrl":"https://doi.org/10.1111/apha.14041","url":null,"abstract":"The increasing prevalence of obesity, prediabetes and type 2 diabetes (T2D) emphasizes the need for a more complete understanding of the mechanisms mediating glucose homeostasis to accelerate the identification of new medications to prevent conversion to T2D. Recent reports indicate that former obesity medication, 5-hydroxytryptamine (5-HT, serotonin)2C receptor (5-HT 2C R) agonist lorcaserin improves glycemic control in association with weight loss in obese patients with T2D. We examined whether lorca-serin has a direct effect on insulin sensitivity and how this effect is achieved. We clarify that lorcaserin dose-dependently improves glycemic control in a mouse model of T2D without altering body weight. Examining the mechanism of this effect, we reveal a necessary and sufficient neuro-chemical mediator of lorcaserin’s glucoregulatory effects, via activation of brain pro-opiomelanocortin (POMC) peptides. We observed that lorcaserin reduces hepatic glucose production and improves insulin sensitivity. The recent large scale clinical trial CAMELLIA-TIMI 61 revealed that lorcaserin prevented conversion to T2D and improved T2D and supports the translational relevance this medication for prediabetes and T2D treatment. Taken together, these data suggest that lorcaserin’s action within the brain represents a mechanistically novel treatment for prediabetes and T2D: findings of significance to a prevalent global disease.","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 S728","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"6869267","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":"New insights into the molecular basis of how physical activity contributes to human health","authors":"Anika Westphal","doi":"10.1111/apha.14047","DOIUrl":"10.1111/apha.14047","url":null,"abstract":"<p>Physical exercise is beneficial for maintaining human health. Daily physical activity and balanced nutrition are recommended by the WHO.<span><sup>1-4</sup></span> Regular exercise training is recommended at any age and reduces the risk for many chronic metabolic diseases like neurodegenerative and cardiovascular diseases, type 2 diabetes, cancer, and neuronal dysfunctions.<span><sup>2, 5</sup></span> The positive effects of regular exercise include improved insulin sensitivity, increased maximal oxygen uptake, reduced adiposity, less systemic inflammation, and improved bone strength. The underlying molecular biological mechanisms have not yet been fully elucidated.<span><sup>4</sup></span> This report summarizes articles and new research findings about skeletal muscles, physical activity, and its contribution to human health, recently published in <i>Acta Physiologica</i>.</p><p>Whether someone is sporty or not depends on many factors. In endurance sports, becoming a successful professional athlete is also hereditary. Kenyan runners belong to the elite middle- and long-distance runners, with Eliud Kipchoge on the top. Kunimasa et al. compared the influence of leg and foot segmental length and muscle–tendon architecture of Kenyans and Japanese males regarding their potential to be an elite middle- and long-distance runner. It was shown that not only Kenyan runners but also the general Kenyan population, compared with the Japanese, have structural advantages in leg composition and muscle–tendon architecture from early childhood.<span><sup>6</sup></span>\u0000 </p><p>Athletic performance can be improved via different strategies. One is supplementation with nutritions. Bioactive peptides, like collagen, have systemic beneficial properties, for example, antihypertensive, antimicrobial, immunomodulatory, and antioxidant effects. Balshaw et al. focused on the question whether the supplementation of bioactive collagen peptides, compared with a placebo, improves skeletal muscle strength, size and architecture by resistance training. Therefore, young healthy men underwent a standardized program of resistance training supplemented by either collagen peptides or placebo. They found that on the one hand muscle strength did not increase compared with the control group. On the other hand, resistance training and collagen peptide supplementation positively influenced skeletal muscle remodeling, for example, greater percentage changes in the total volume of muscles exercised, the volume of the quadriceps, and a greater increase in the vastus medialis muscle.<span><sup>7</sup></span>\u0000 </p><p>Another method to improve training effects is described by Christiansen et al. Since 2021, a novel popular training method for top athletes is blood-flow-restricted (BFR)-exercise. Muscle blood flow gets reduced by inflating pressure cuffs around the limbs. The research team focused on the question whether BFR exercise could be a potential treatment for me","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202297","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":"Glomerular microcirculation: Implications for diabetes, preeclampsia, and kidney injury","authors":"Michael S. Goligorsky","doi":"10.1111/apha.14048","DOIUrl":"10.1111/apha.14048","url":null,"abstract":"<p>This review outlines the features of tandem regulation of glomerular microcirculation by autoregulatory mechanisms and intraglomerular redistribution of blood flow. Multiple points of cooperation exist between autoregulatory and distributional mechanisms. Mutual interactions between myogenic and tubuloglomerular feedback (TGF) mechanisms regulating the inflow are briefly discussed. In addition to this, TGF operation involving purinergic, autocoid, and NO signaling affects, however, not only afferent arteriolar tone, but mesangial cell tone as well. The latter reversibly reconfigures the distribution of blood flow between the shorter and longer pathways in the glomerular tuft. I advance a hypothesis that blood flow in these pathways spontaneously alternates, and mesangial cell tonicity serves as a rheostatic shift between them. Furthermore, humoral messengers from macula densa cells, themselves dependent on myogenic mechanisms, fine-tune the secretion of renin and, subsequently, the local, intrarenal generation of angiotensin II, which, in turn, provides additional vasomotor signaling to glomerular capillaries through changing the tone of mesangial cells. This complex regulatory network may partially explain the phenomenon of renal functional reserve, as well as suggest implications for changes in renal function during pregnancy, early diabetes mellitus, and acute kidney injury.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 3","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10190990","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":"Retraction statement: Role of the immune system in vascular function and blood pressure control induced by faecal microbiota transplantation in rats","authors":"","doi":"10.1111/apha.14039","DOIUrl":"10.1111/apha.14039","url":null,"abstract":"<p>Toral, M, Robles-Vera, I, de la Visitación, N, et al. Role of the immune system in vascular function and blood pressure control induced by faecal microbiota transplantation in rats. <i>Acta Physiol</i>. 2019; 227:e13285. https://doi.org/10.1111/apha.13285.</p><p>The above article, published online on April 20, 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor in Chief, Pontus B. Persson, the Scandinavian Physiological Society, and John Wiley and Sons Ltd. The retraction has been agreed due to the similarity of a figure and inconsistencies regarding underlying data between this article and the following article published in <i>Front Physiol</i>, “Critical Role of the Interaction Gut Microbiota–Sympathetic Nervous System in the Regulation of Blood Pressure” by Toral M, Robles-Vera I, de la Visitación N, et al., 2019; 10:231. doi: 10.3389/fphys.2019.00231.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 4","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10137875","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":"Endothelial cell plasticity in kidney fibrosis and disease","authors":"Layla Pohl,&nbsp;Ina Maria Schiessl","doi":"10.1111/apha.14038","DOIUrl":"10.1111/apha.14038","url":null,"abstract":"<p>Renal endothelial cells demonstrate an impressive remodeling potential during angiogenic sprouting, vessel repair or while transitioning into mesenchymal cells. These different processes may play important roles in both renal disease progression or regeneration while underlying signaling pathways of different endothelial cell plasticity routes partly overlap. Angiogenesis contributes to wound healing after kidney injury and pharmaceutical modulation of angiogenesis may home a great therapeutic potential. Yet, it is not clear whether any differentiated endothelial cell can proliferate or whether regenerative processes are largely controlled by resident or circulating endothelial progenitor cells. In the glomerular compartment for example, a distinct endothelial progenitor cell population may remodel the glomerular endothelium after injury. Endothelial-to-mesenchymal transition (EndoMT) in the kidney is vastly documented and often associated with endothelial dysfunction, fibrosis, and kidney disease progression. Especially the role of EndoMT in renal fibrosis is controversial. Studies on EndoMT in vivo determined possible conclusions on the pathophysiological role of EndoMT in the kidney, but whether endothelial cells really contribute to kidney fibrosis and if not what other cellular and functional outcomes derive from EndoMT in kidney disease is unclear. Sequencing data, however, suggest no participation of endothelial cells in extracellular matrix deposition. Thus, more in-depth classification of cellular markers and the fate of EndoMT cells in the kidney is needed. In this review, we describe different signaling pathways of endothelial plasticity, outline methodological approaches and evidence for functional and structural implications of angiogenesis and EndoMT in the kidney, and eventually discuss controversial aspects in the literature.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10519388","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":"GDF15 mediates renal cell plasticity in response to potassium depletion in mice","authors":"Samia Lasaad,&nbsp;Christine Walter,&nbsp;Chloé Rafael,&nbsp;Luciana Morla,&nbsp;Alain Doucet,&nbsp;Nicolas Picard,&nbsp;Anne Blanchard,&nbsp;Yves Fromes,&nbsp;Béatrice Matot,&nbsp;Gilles Crambert,&nbsp;Lydie Cheval","doi":"10.1111/apha.14046","DOIUrl":"10.1111/apha.14046","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To understand the mechanisms involved in the response to a low-K⁺ diet (LK), we investigated the role of the growth factor GDF15 and the ion pump H,K-ATPase type 2 (HKA2) in this process.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Male mice of different genotypes (WT, GDF15-KO, and HKA2-KO) were fed an LK diet for different periods of time. We analyzed GDF15 levels, metabolic and physiological parameters, and the cellular composition of collecting ducts.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Mice fed an LK diet showed a 2–4-fold increase in plasma and urine GDF15 levels. Compared to WT mice, GDF15-KO mice rapidly developed hypokalemia due to impaired renal adaptation. This is related to their 1/ inability to increase the number of type A intercalated cells (AIC) and 2/ absence of upregulation of H,K-ATPase type 2 (HKA2), the two processes responsible for K⁺ retention. Interestingly, we showed that the GDF15-mediated proliferative effect on AIC was dependent on the ErbB2 receptor and required the presence of HKA2. Finally, renal leakage of K⁺ induced a reduction in muscle mass in GDF15-KO mice fed LK diet.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In this study, we showed that GDF15 and HKA2 are linked and play a central role in the response to K⁺ restriction by orchestrating the modification of the cellular composition of the collecting duct.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202668","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 role of the mesangium in glomerular function","authors":"Roberto Boi,&nbsp;Kerstin Ebefors,&nbsp;Jenny Nyström","doi":"10.1111/apha.14045","DOIUrl":"10.1111/apha.14045","url":null,"abstract":"<p>When discussing glomerular function, one cell type is often left out, the mesangial cell (MC), probably since it is not a part of the filtration barrier per se. The MCs are instead found between the glomerular capillaries, embedded in their mesangial matrix. They are in direct contact with the endothelial cells and in close contact with the podocytes and together they form the glomerulus. The MCs can produce and react to a multitude of growth factors, cytokines, and other signaling molecules and are in the perfect position to be a central hub for crosstalk communication between the cells in the glomerulus. In certain glomerular diseases, for example, in diabetic kidney disease or IgA nephropathy, the MCs become activated resulting in mesangial expansion. The expansion is normally due to matrix expansion in combination with either proliferation or hypertrophy. With time, this expansion can lead to fibrosis and decreased glomerular function. In addition, signs of complement activation are often seen in biopsies from patients with glomerular disease affecting the mesangium. This review aims to give a better understanding of the MCs in health and disease and their role in glomerular crosstalk and inflammation.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10492460","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":"Global proteomics reveals insulin abundance as a marker of human islet homeostasis alterations","authors":"Andreas F. Mathisen,&nbsp;Shadab Abadpour,&nbsp;Thomas Aga Legøy,&nbsp;Joao A. Paulo,&nbsp;Luiza Ghila,&nbsp;Hanne Scholz,&nbsp;Simona Chera","doi":"10.1111/apha.14037","DOIUrl":"10.1111/apha.14037","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>The variation in quality between the human islet samples represents a major problem for research, especially when used as control material. The assays assessing the quality of human islets used in research are non-standardized and limited, with many important parameters not being consistently assessed. High-throughput studies aimed at characterizing the diversity and segregation markers among apparently functionally healthy islet preps are thus a requirement. Here, we designed a pilot study to comprehensively identify the diversity of global proteome signatures and the deviation from normal homeostasis in randomly selected human-isolated islet samples.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>By using Tandem Mass Tag 16-plex proteomics, we focused on the recurrently observed disparity in the detected insulin abundance between the samples, used it as a segregating parameter, and analyzed the correlated changes in the proteome signature and homeostasis by pathway analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this pilot study, we showed that insulin protein abundance is a predictor of human islet homeostasis and quality. This parameter is independent of other quality predictors within their acceptable range, thus being able to further stratify islets samples of apparent good quality. Human islets with low amounts of insulin displayed changes in their metabolic and signaling profile, especially in regard to energy homeostasis and cell identity maintenance. We further showed that xenotransplantation into diabetic hosts is not expected to improve the pre-transplantation signature, as it has a negative effect on energy balance, antioxidant activity, and islet cell identity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Insulin protein abundance predicts significant changes in human islet homeostasis among random samples of apparently good quality.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10423139","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":"Detecting and exploiting the circadian clock in rheumatoid arthritis","authors":"Siska Wilantri,&nbsp;Hanna Grasshoff,&nbsp;Tanja Lange,&nbsp;Timo Gaber,&nbsp;Luciana Besedovsky,&nbsp;Frank Buttgereit","doi":"10.1111/apha.14028","DOIUrl":"10.1111/apha.14028","url":null,"abstract":"<p>Over the past four decades, research on 24-h rhythms has yielded numerous remarkable findings, revealing their genetic, molecular, and physiological significance for immunity and various diseases. Thus, circadian rhythms are of fundamental importance to mammals, as their disruption and misalignment have been associated with many diseases and the abnormal functioning of many physiological processes. In this article, we provide a brief overview of the molecular regulation of 24-h rhythms, their importance for immunity, the deleterious effects of misalignment, the link between such pathological rhythms and rheumatoid arthritis (RA), and the potential exploitation of chronobiological rhythms for the chronotherapy of inflammatory autoimmune diseases, using RA as an example.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10054254","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":"Neuroglia: Function and Pathology by Alexei Verkhratsky and Arthur M. Butt","authors":"Tibor Harkany,&nbsp;Tomas Hökfelt","doi":"10.1111/apha.14033","DOIUrl":"10.1111/apha.14033","url":null,"abstract":"&lt;p&gt;“Glial cells are in the brain to support neurons” is one of the commonplaces taught at regular lectures by neuroscientists to future generations of neurobiologists. Never mind that detailed insights into glial physiology and pathobiology are usually neglected in thematic neuroscience curricula. Indeed, the classic bias in the field of neuroscience comes from the term “neuro” itself. General thinking dictates that when one can manipulate specific subtypes of neurons distinguished by a signature of probably a handful of molecules at millisecond precision chemically or by light, and receive a behavioral response from the experimental organism, be this invertebrate or vertebrate, then neurons alone shall be sufficient to organize the brain's output. We could not be more wrong and on an arduous journey to fundamentally misinterpret brain operations if holding onto these views. It is time to acknowledge the contribution of other cell types, cumulatively termed “neuroglia,” with astroglia, oligodendroglia, and microglia being present in the central nervous system alone. Adding Schwann cells, satellite glia, enteric glia, and glial cells of sensory organs to this list is a thrilling reminder that an amazing variety of glial cell types not only exists at around 1:1 ratio but works in unison in the human nervous systems to allow it to reach its computational, intellectual, and emotional power that makes us unique.&lt;/p&gt;&lt;p&gt;“Would you know a renown ‘glioscientist’ as if a neuroscientist?” For many, this could be an unexpectedly challenging question still. Here, we introduce &lt;b&gt;Alexei Verkhratsky&lt;/b&gt; and &lt;b&gt;Arthur M. Butt&lt;/b&gt; as two of the most eminent glia biologists of our time whose new book, titled “&lt;b&gt;Neuroglia: Function and Pathology&lt;/b&gt;” is a wonderfully illustrated, comprehensive, thematic, and insightful account of the vast knowledge that has accumulated on glial cells of both the central and peripheral nervous systems over the past ~150 years. This book, the newest in a series of compendia on glial cells,&lt;span&gt;&lt;sup&gt;1-4&lt;/sup&gt;&lt;/span&gt; is educational for it systematically summarizing the origins, development, anatomy, molecular make-up, membrane biophysics, cellular interactions, and functions in relation to nerve cells and the broader brain homeostasis of each major glial cell type. Yet, it is an enticing read that also answers many unexpected questions ranging from the history of neuroscience (e.g., “do you know who coined the word astrocyte?”) to debunking some of the most pressing dogmas, like the number of neurons versus other cells in the brain. To this point, and using even evolutionary biology, a ~ 1:1 neuron: astrocyte ratio is formulated, which could work well if one considers that each neuron could have its “personal” caretaker, which supports, interacts, facilitates, removes waste, and even protects against disease and demise.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Neuroglia: Function and Pathology&lt;/b&gt; starts with a historical account of discoveries that shaped this fie","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"239 2","pages":""},"PeriodicalIF":6.3,"publicationDate":"2023-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10037236","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}