Acta Physiologica最新文献

{"title":"Postnatal development of vasoactive intestinal polypeptide-expressing GABAergic interneurons in mouse somatosensory cortex","authors":"Clara A. Simacek,&nbsp;Sergei Kirischuk,&nbsp;Thomas Mittmann","doi":"10.1111/apha.14265","DOIUrl":"10.1111/apha.14265","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Despite dysfunctional vasoactive intestinal polypeptide-positive interneurons (VIP-INs) being linked to the emergence of neurodevelopmental disorders, the temporal profile of VIP-IN functional maturation and cortical network integration remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Postnatal VIP-IN development was traced with patch clamp experiments in the somatosensory cortex of <i>Vip-IRES-cre x tdTomato</i> mice. Age groups were chosen during barrel field formation, before and after activation of main sensory inputs, and in adult animals (postnatal days (P) P3–4, P8–10, P14–16, and P30–36).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Changes in passive and active membrane properties show a maturation towards accelerated signal integrations. Excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) showed progressive VIP-IN integration into cortical networks, likely via synaptogenesis: mEPSC frequency increased before P8–10, while mIPSC frequency increased at P14–16. Only mIPSC kinetics became accelerated, and the <i>E</i>/<i>I</i> ratio of synaptic inputs, defined as a ratio of mEPSC to mIPSC charge transfer, remained constant throughout the investigated developmental stages. Evoked (e)EPSCs and (e)IPSCs showed increased amplitudes, while only eIPSCs demonstrated faster kinetics. eEPSCs and eIPSCs revealed a paired-pulse facilitation by P14–16, indicating probably a decrease in the presynaptic release probability (<i>p</i>_<i>r</i>) and a paired-pulse depression in adulthood. eIPSCs also showed the latter, suggesting a decrease in <i>p</i>_<i>r</i> for both signal transmission pathways at this time point.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>VIP-INs mature towards faster signal integration and pursue different strategies to avoid overexcitation. Excitatory and inhibitory synaptic transmission become stronger and shorter via different pre- and postsynaptic alterations, likely promoting the execution of active whisking.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968858","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":"Real-time detection of somatostatin release from single islets reveals hypersecretion in type 2 diabetes","authors":"Mingyu Yang,&nbsp;Kousik Mandal,&nbsp;Moa Södergren,&nbsp;Özge Dumral,&nbsp;Lena Winroth,&nbsp;Anders Tengholm","doi":"10.1111/apha.14268","DOIUrl":"10.1111/apha.14268","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Somatostatin from pancreatic δ-cells is a paracrine regulator of insulin and glucagon secretion, but the release kinetics and whether secretion is altered in diabetes is unclear. This study aimed to improve understanding of somatostatin secretion by developing a tool for real-time detection of somatostatin release from individual pancreatic islets.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Reporter cells responding to somatostatin with cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i) changes were generated by co-expressing somatostatin receptor SSTR2, the G-protein Gα15 and a fluorescent Ca²⁺ sensor in HeLa cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Somatostatin induced dose-dependent [Ca²⁺]_i increases in reporter cells with half-maximal and maximal effects at 1.6 ± 0.4 and ~30 nM, respectively. Mouse and human islets induced reporter cell [Ca²⁺]_i elevations that were inhibited by the SSTR2 antagonist CYN154806. Depolarization of islets by high K⁺, K_ATP channel blockade or increasing the glucose concentration from 3 to 11 mM evoked concomitant elevations of [Ca²⁺]_i in islets and reporter cells. Exposure of islets to glucagon, GLP-1 and ghrelin also triggered reporter cell [Ca²⁺]_i responses, whereas little effect was obtained by islet exposure to insulin, glutamate, GABA and urocortin-3. Islets from type 2 diabetic human donors induced higher reporter cell [Ca²⁺]_i responses at 11 mM and after K⁺ depolarization compared with non-diabetic islets, although fewer δ-cells were identified by immunostaining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Type 2 diabetes is associated with hypersecretion of somatostatin, which has implications for paracrine regulation of insulin and glucagon secretion. The new reporter cell assay for real-time detection of single-islet somatostatin release holds promise for further studies of somatostatin secretion in islet physiology and pathophysiology.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968868","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":"Left superior cervical ganglia lymph node mimicry and its role in rat ventricular arrhythmias following myocardial infarction","authors":"Qingxia Yu,&nbsp;Yan Li,&nbsp;Wenju Yan,&nbsp;Weizhong Han,&nbsp;Qian Liu,&nbsp;Junyi Zhang,&nbsp;Xiaolu Li,&nbsp;Yugen Shi,&nbsp;Yu Wang,&nbsp;Jie Yin,&nbsp;Suhua Yan","doi":"10.1111/apha.14279","DOIUrl":"10.1111/apha.14279","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Sympathetic overactivation may lead to severe ventricular arrhythmias (VAs) post-myocardial infarction (MI). The superior cervical ganglion (SCG) is an extracardiac sympathetic ganglion which regulates cardiac autonomic tone. We aimed to investigate the characteristics and functional significance of SCG on neuro-cardiac communication post-MI.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Constructed MI rat model by left anterior descending coronary artery ligation, and electrophysiological, SCG sympathetic nerve activity testing, echocardiography and histology study were performed. The proteins and gene expression were detected using RNA-seq, spatial transcriptomics, quantitative PCR, and western blotting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The SCG neuronal remodeling was recognized by significant increase in adrenergic tyrosine hydroxylase (TH) (+) neurons and decrease in neuronal size. Top differentially expressed genes enriched in pro-inflammatory profile and nerve regulatory factor in left SCG (LSCG) post-MI. Interleukin (IL)-1β and IL-6 increased significantly at Day 3, ahead of nerve growth factor (NGF) which peaked at Day 7 post-MI. Spatial transcriptomics further identified the relativity of TH enrichment with macrophages and cytokines. Therapeutic LSCG-ectomy successfully triggered cardiac denervation and improved VA vulnerability. Eventually, cardiac denervation attenuated macrophage/mast cell infiltration at para-infarct regions, thus improved cardiac dysfunction. Mechanism study revealed that genetic knockdown of NGF receptor trkA in LSCG reversed sympathetic remodeling and cardiac inflammation, which may be partially mediated by substance P and calcitonin gene-related peptide (CGRP).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Extracardiac sympathetic LSCG remodeling participated in arrhythmogenesis and cardiac inflammation/function post-MI. NGF bridged neuro-immune crosstalk between pro-inflammatory shifting and sympathetic overdrive. Targeting LSCG modification facilitated cardiac protection and prevented VAs post-MI.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968854","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":"Oral presentations","authors":"","doi":"10.1111/apha.14253","DOIUrl":"10.1111/apha.14253","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 S732","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.14253","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976741","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":"IgE and cardiac disease","authors":"Scott P. Levick","doi":"10.1111/apha.14281","DOIUrl":"10.1111/apha.14281","url":null,"abstract":"<p>IgE acts primarily via the high affinity IgE receptor (FcεRI) and is central to immediate hypersensitivity reactions (anaphylaxis). However, IgE is also important in the development of chronic hypersensitivity reactions (allergy). In the cardiovascular system, numerous clinical studies have investigated serum IgE levels, mainly in the context of myocardial infarction, and have established a clear association between IgE and ischemic cardiac events. While animal studies demonstrate that IgE can cause atherosclerotic plaque formation, this is complicated by clinical reports that IgE is associated with non-fatal ischemic events and not with fatal events, raising the possibility that IgE could be protective in this setting. In terms of non-ischemic cardiac disease, little information is available clinically for IgE; however, animal models also indicate that IgE promotes adverse effects in this setting as well. This review article will present the clinical studies that have established a relationship between serum IgE levels and cardiac disease, particularly myocardial infarction. This review article will also discuss animal studies that provide mechanistic understanding of how IgE can exert chronic effects in the heart. This article also attempts to address the question of whether IgE is causative of cardiac disease or is a response to cardiac disease.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968851","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":"Potential role of signal transducer and activator of transcription 3 in the amygdala in mitigating stress-induced high blood pressure via exercise in rats","authors":"Keisuke Tomita,&nbsp;Ko Yamanaka,&nbsp;Thu Van Nguyen,&nbsp;Jimmy Kim,&nbsp;Linh Thuy Pham,&nbsp;Toru Kobayashi,&nbsp;Sabine S. Gouraud,&nbsp;Hidefumi Waki","doi":"10.1111/apha.14274","DOIUrl":"10.1111/apha.14274","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Chronic stress elevates blood pressure, whereas regular exercise exerts antistress and antihypertensive effects. However, the mechanisms of stress-induced hypertension and preventive effects through exercise remain unknown. Thus, we investigated the molecular basis involved in autonomic blood pressure regulation within the amygdala.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The effects of a 3-week restraint stress and daily voluntary exercise against stress on cardiovascular parameters and gene expression profiles in the amygdala were examined using a microarray method. Candidate genes were selected from differentially expressed genes; the localization of their expression within the central nucleus of the amygdala and their roles in cardiovascular regulation were examined using small-interfering RNA transfection and radiotelemetry.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Chronic restraint stress caused an increase in blood pressure levels; however, with voluntary exercise, the blood pressure levels remained comparable to those of the controls. Compared with the controls, chronic restraint stress decreased signal transducer and activator of transcription 3 expression in the amygdala, whereas voluntary exercise improved its expression to normal levels. Immunohistochemical staining revealed the expression of signal transducer and activator of transcription 3 in neurons of the amygdala; inhibition of this expression using small-interfering RNA increased the arterial pressure. However, spontaneous baroreflex gain and low- and high-frequency components of heart rate variability remained unaffected by the inhibition of signal transducer and activator of transcription 3.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In the amygdala, signal transducer and activator of transcription 3 regulates the blood pressure levels and is possibly involved in blood pressure elevation in response to chronic stress and its improvement by voluntary exercise.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968861","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":"Prebiotics as modulators of colonic calcium and magnesium uptake","authors":"Friederike Stumpff,&nbsp;David Manneck","doi":"10.1111/apha.14262","DOIUrl":"10.1111/apha.14262","url":null,"abstract":"<p>Ca²⁺ and Mg²⁺ are essential nutrients, and deficiency can cause serious health problems. Thus, lack of Ca²⁺ and Mg²⁺ can lead to osteoporosis, with incidence rising both in absolute and age-specific terms, while Mg²⁺ deficiency is associated with type II diabetes. Prevention via vitamin D or estrogen is controversial, and the bioavailability of Ca²⁺ and Mg²⁺ from supplements is significantly lower than that from milk products. Problems are likely to increase as populations age and the number of people on vegan diets surges. Developing new therapeutic strategies requires a better understanding of the molecular mechanisms involved in absorption by intestinal epithelia. The vitamin-D dependent, active pathway for the uptake of Ca²⁺ from the upper small intestine involving TRPV6 is highly efficient but only accounts for about 20% of total uptake. Instead, most Ca²⁺ uptake is thought to occur via passive paracellular diffusion across the ileum, although sufficiently high luminal concentrations are difficult to achieve.. Interestingly, colon and caecum also have a considerable capacity for the active absorption of Ca²⁺ and Mg²⁺, the molecular mechanisms of which are unclear. Intriguingly, stimulating fermentation by prebiotics enhances colonic absorption, which can rise from ~10% to ~30% of the total. Notably, fermentation releases protons, which inhibits channels highly selective for Ca²⁺ and Mg²⁺ (TRPV6 and TRPM6/TRPM7). Conversely, the non-selective cation channel TRPV3 is stimulated by both intracellular acidification and by numerous herbal compounds. Spicy, fiber-rich food, as traditionally consumed in many cultures, might enhance the uptake of Ca²⁺ and Mg²⁺ via this pathway.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968865","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":"Ultrafast multicellular calcium imaging of calcium spikes in mouse beta cells in tissue slices","authors":"Jurij Dolenšek,&nbsp;Viljem Pohorec,&nbsp;Maša Skelin Klemen,&nbsp;Marko Gosak,&nbsp;Andraž Stožer","doi":"10.1111/apha.14261","DOIUrl":"10.1111/apha.14261","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The crucial steps in beta cell stimulus-secretion coupling upon stimulation with glucose are oscillatory changes in metabolism, membrane potential, intracellular calcium concentration, and exocytosis. The changes in membrane potential consist of bursts of spikes, with silent phases between them being dominated by membrane repolarization and absence of spikes. Assessing intra- and intercellular coupling at the multicellular level is possible with ever-increasing detail, but our current ability to simultaneously resolve spikes from many beta cells remains limited to double-impalement electrophysiological recordings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Since multicellular calcium imaging of spikes would enable a better understanding of coupling between changes in membrane potential and calcium concentration in beta cell collectives, we set out to design an appropriate methodological approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Combining the acute tissue slice method with ultrafast calcium imaging, we were able to resolve and quantify individual spikes within bursts at a temporal resolution of &gt;150 Hz over prolonged periods, as well as describe their glucose-dependent properties. In addition, by simultaneous patch-clamp recordings we were able to show that calcium spikes closely follow membrane potential changes. Both bursts and spikes coordinate across islets in the form of intercellular waves, with bursts typically displaying global and spikes more local patterns.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This method and the associated findings provide additional insight into the complex signaling within beta cell networks. Once extended to tissue from diabetic animals and human donors, this approach could help us better understand the mechanistic basis of diabetes and find new molecular targets.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968900","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":"Chronodisruption that dampens output of the central clock abolishes rhythms in metabolome profiles and elevates acylcarnitine levels in the liver of female rats","authors":"Shiyana Arora,&nbsp;Pavel Houdek,&nbsp;Tomáš Čajka,&nbsp;Tereza Dočkal,&nbsp;Martin Sládek,&nbsp;Alena Sumová","doi":"10.1111/apha.14278","DOIUrl":"10.1111/apha.14278","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Exposure to light at night and meal time misaligned with the light/dark (LD) cycle—typical features of daily life in modern 24/7 society—are associated with negative effects on health. To understand the mechanism, we developed a novel protocol of complex chronodisruption (CD) in which we exposed female rats to four weekly cycles consisting of 5-day intervals of constant light and 2-day intervals of food access restricted to the light phase of the 12:12 LD cycle.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We examined the effects of CD on behavior, estrous cycle, sleep patterns, glucose homeostasis and profiles of clock- and metabolism-related gene expression (using RT qPCR) and liver metabolome and lipidome (using untargeted metabolomic and lipidomic profiling).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CD attenuated the rhythmic output of the central clock in the suprachiasmatic nucleus via <i>Prok2</i> signaling, thereby disrupting locomotor activity, the estrous cycle, sleep patterns, and mutual phase relationship between the central and peripheral clocks. In the periphery, CD abolished <i>Per1,2</i> expression rhythms in peripheral tissues (liver, pancreas, colon) and worsened glucose homeostasis. In the liver, it impaired the expression of NAD⁺, lipid, and cholesterol metabolism genes and abolished most of the high-amplitude rhythms of lipids and polar metabolites. Interestingly, CD abolished the circadian rhythm of <i>Cpt1a</i> expression and increased the levels of long-chain acylcarnitines (ACar 18:2, ACar 16:0), indicating enhanced fatty acid oxidation in mitochondria.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our data show the widespread effects of CD on metabolism and point to ACars as biomarkers for CD due to misaligned sleep and feeding patterns.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968891","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":"Transient receptor potential melastatin 7 cation channel, magnesium and cell metabolism in vascular health and disease","authors":"Belma Melda Abidin,&nbsp;Francisco J. Rios,&nbsp;Augusto C. Montezano,&nbsp;Rhian M. Touyz","doi":"10.1111/apha.14282","DOIUrl":"10.1111/apha.14282","url":null,"abstract":"<p>Preserving the balance of metabolic processes in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), is crucial for optimal vascular function and integrity. ECs are metabolically active and depend on aerobic glycolysis to efficiently produce energy for their essential functions, which include regulating vascular tone. Impaired EC metabolism is linked to endothelial damage, increased permeability and inflammation. Metabolic alterations in VSMCs also contribute to vascular dysfunction in atherosclerosis and hypertension. Magnesium (Mg²⁺) is the second most abundant intracellular divalent cation and influences molecular processes that regulate vascular function, including vasodilation, vasoconstriction, and release of vasoactive substances. Mg²⁺ is critically involved in maintaining cellular homeostasis and metabolism since it is an essential cofactor for ATP, nucleic acids and hundreds of enzymes involved in metabolic processes. Low Mg²⁺ levels have been linked to endothelial dysfunction, increased vascular tone, vascular inflammation and arterial remodeling. Growing evidence indicates an important role for the transient receptor potential melastatin-subfamily member 7 (TRPM7) cation channel in the regulation of Mg²⁺ homeostasis in EC and VSMCs. In the vasculature, TRPM7 deficiency leads to impaired endothelial function, increased vascular contraction, phenotypic switching of VSMCs, inflammation and fibrosis, processes that characterize the vascular phenotype in hypertension. Here we provide a comprehensive overview on TRPM7/Mg²⁺ in the regulation of vascular function and how it influences EC and VSMC metabolism such as glucose and energy homeostasis, redox regulation, phosphoinositide signaling, and mineral metabolism. The putative role of TRPM7/Mg²⁺ and altered cellular metabolism in vascular dysfunction and hypertension is also discussed.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 2","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143055751","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}