Acta Physiologica最新文献

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Deuterated water (2H2O) can be used to quantify hemoglobin synthesis and red blood cell lifespan in humans. 氘化水(2H2O)可用于定量人体血红蛋白合成和红细胞寿命。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-02-01 Epub Date: 2024-12-20 DOI: 10.1111/apha.14259
Hilkka Kontro, Chris McGlory, Martin J MacInnis
{"title":"Deuterated water (<sup>2</sup>H<sub>2</sub>O) can be used to quantify hemoglobin synthesis and red blood cell lifespan in humans.","authors":"Hilkka Kontro, Chris McGlory, Martin J MacInnis","doi":"10.1111/apha.14259","DOIUrl":"10.1111/apha.14259","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14259"},"PeriodicalIF":5.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862618","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}
引用次数: 0
Supplement: 7th Congress of Physiology and Integrative Biology, 91st Congress of French Physiological Society, Tours, France, 5-7 June, 2024. 补编:第7届生理学与综合生物学大会,第91届法国生理学会大会,图尔,法国,2024年6月5-7日。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 DOI: 10.1111/apha.14252
{"title":"Supplement: 7th Congress of Physiology and Integrative Biology, 91st Congress of French Physiological Society, Tours, France, 5-7 June, 2024.","authors":"","doi":"10.1111/apha.14252","DOIUrl":"https://doi.org/10.1111/apha.14252","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 Suppl 732 ","pages":"e14252"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976736","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}
引用次数: 0
High chloride induces aldosterone resistance in the distal nephron. 高氯化物诱导远端肾小球的醛固酮抵抗。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-10-24 DOI: 10.1111/apha.14246
Helga Vitzthum, Nina Hauswald, Helena Pham, Leya Eckermann-Reimer, Catherine Meyer-Schwesinger, Heimo Ehmke
{"title":"High chloride induces aldosterone resistance in the distal nephron.","authors":"Helga Vitzthum, Nina Hauswald, Helena Pham, Leya Eckermann-Reimer, Catherine Meyer-Schwesinger, Heimo Ehmke","doi":"10.1111/apha.14246","DOIUrl":"10.1111/apha.14246","url":null,"abstract":"<p><strong>Aim: </strong>Increasing the dietary intake of K<sup>+</sup> in the setting of a high salt intake promotes renal Na<sup>+</sup> excretion even though K<sup>+</sup> concurrently enhances the secretion of aldosterone, the most effective stimulus for renal Na<sup>+</sup> reabsorption. Here, we questioned whether in the high salt state a mechanism exists, which attenuates the aldosterone response to prevent renal Na<sup>+</sup> reabsorption after high K<sup>+</sup> intake.</p><p><strong>Methods: </strong>Mice were fed diets containing varying amounts of Na<sup>+</sup> combined with KCl or KCitrate. Murine cortical connecting duct (mCCDcl1) cells were cultured in media containing normal or high [Cl<sup>-</sup>]. The response to aldosterone was analyzed by high-resolution imaging and by biochemical approaches.</p><p><strong>Results: </strong>The canonical cellular response to aldosterone, encompassing translocation of the mineralocorticoid receptor (MR) and activation of the epithelial Na<sup>+</sup> channel ENaC was repressed in Na<sup>+</sup>-replete mice fed a high KCl diet, even though plasma aldosterone concentrations were increased. The response to aldosterone was restored in Na<sup>+</sup>-replete mice when the extracellular [Cl<sup>-</sup>] increase was prevented by feeding a high KCitrate diet. In mCCDcl1 cells, an elevated extracellular [Cl<sup>-</sup>] was sufficient to disrupt the aldosterone-induced MR translocation.</p><p><strong>Conclusion: </strong>These findings indicate a pivotal role for extracellular [Cl<sup>-</sup>] in modulating renal aldosterone signaling to adapt MR activation by a high K<sup>+</sup> intake to the NaCl balance. An impairment of [Cl<sup>-</sup>]-mediated aldosterone resistance may contribute to excessive MR activation by aldosterone in the presence of a high salt intake characteristic of the Western diet, resulting in an inappropriate salt reabsorption and its downstream detrimental effects.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14246"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11674995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491350","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}
引用次数: 0
Correction to "Beneficial effects of MGL-3196 and BAM15 combination in a mouse model of fatty liver disease". 更正 "MGL-3196 和 BAM15 联合疗法在脂肪肝小鼠模型中的益处"。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-11-12 DOI: 10.1111/apha.14250
{"title":"Correction to \"Beneficial effects of MGL-3196 and BAM15 combination in a mouse model of fatty liver disease\".","authors":"","doi":"10.1111/apha.14250","DOIUrl":"10.1111/apha.14250","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14250"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612905","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}
引用次数: 0
A potential link between enteric glia and the pathophysiology of diet-induced obesity and related metabolic diseases. 肠胶质细胞与饮食引起的肥胖和相关代谢疾病的病理生理之间的潜在联系。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-12-06 DOI: 10.1111/apha.14258
Onesmo B Balemba, Brian D Gulbransen
{"title":"A potential link between enteric glia and the pathophysiology of diet-induced obesity and related metabolic diseases.","authors":"Onesmo B Balemba, Brian D Gulbransen","doi":"10.1111/apha.14258","DOIUrl":"10.1111/apha.14258","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14258"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142783358","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}
引用次数: 0
Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice. 抑制组蛋白去乙酰化酶 6 可促进微管乙酰化,并有助于肌营养不良 mdx 小鼠的自噬体-溶酶体融合。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-10-18 DOI: 10.1111/apha.14243
Akanksha Agrawal, Erin L Clayton, Courtney L Cavazos, Benjamin A Clayton, George G Rodney
{"title":"Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice.","authors":"Akanksha Agrawal, Erin L Clayton, Courtney L Cavazos, Benjamin A Clayton, George G Rodney","doi":"10.1111/apha.14243","DOIUrl":"10.1111/apha.14243","url":null,"abstract":"<p><strong>Aim: </strong>Duchenne muscular dystrophy is a progressive muscle-wasting disease caused by mutations in the dystrophin gene. Despite progress in dystrophin-targeted gene therapies, it is still a fatal disease requiring novel therapeutics that can be used synergistically or alternatively to emerging gene therapy. Defective autophagy and disorganized microtubule networks contribute to dystrophic pathogenesis, yet the mechanisms by which microtubule alterations regulate autophagy remain elusive. The present study was designed to uncover possible mechanisms underpinning the role of microtubules in regulating autophagy in dystrophic mice.</p><p><strong>Methods: </strong>Mdx mice were also supplemented with Tubastatin A, a pharmacological inhibitor of histone deacetylase 6, and pathophysiology was assessed. Mdx mice with a genetic deletion of the Nox-2 scaffolding subunit p47<sup>phox</sup> were used to assess redox dependence on tubulin acetylation.</p><p><strong>Results: </strong>Our data show decreased acetylation of α-tubulin with enhanced histone deacetylase 6 expression. Tubastatin A increases tubulin acetylation and Q-SNARE complex formation but does not alter microtubule organization or density, indicating improved autophagosome-lysosome fusion. Tubastatin A increases the acetylation of peroxiredoxin and protects it from hyper-oxidation, hence modulating intracellular redox status in mdx mice. Tubastatin A reduces muscle damage and enhances force production. Genetic down regulation of Nox2 activity in the mdx mice promotes autophagosome maturation but not autolysosome formation.</p><p><strong>Conclusion: </strong>Our data highlight that autophagy is differentially regulated by redox and acetylation in mdx mice. By improving autophagy through promoting tubulin acetylation, Tubastatin A decreases the dystrophic phenotype and improves muscle function, suggesting a great potential for clinical translation and treating dystrophic patients.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14243"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11680461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142453748","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}
引用次数: 0
Chloride fluxes and GABA release sustain inhibition in the CNS: The role for Bestrophin 1 anion channels. 氯离子通量和 GABA 释放维持中枢神经系统的抑制作用:Bestrophin 1 阴离子通道的作用。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-11-26 DOI: 10.1111/apha.14254
Alexei Verkhratsky, Verena Untiet, Vladimir V Matchkov
{"title":"Chloride fluxes and GABA release sustain inhibition in the CNS: The role for Bestrophin 1 anion channels.","authors":"Alexei Verkhratsky, Verena Untiet, Vladimir V Matchkov","doi":"10.1111/apha.14254","DOIUrl":"10.1111/apha.14254","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14254"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142714896","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}
引用次数: 0
A quantitative analysis of bestrophin 1 cellular localization in mouse cerebral cortex. 小鼠大脑皮层中 bestrophin 1 细胞定位的定量分析
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-10-28 DOI: 10.1111/apha.14245
Michael Di Palma, Wuhyun Koh, C Justin Lee, Fiorenzo Conti
{"title":"A quantitative analysis of bestrophin 1 cellular localization in mouse cerebral cortex.","authors":"Michael Di Palma, Wuhyun Koh, C Justin Lee, Fiorenzo Conti","doi":"10.1111/apha.14245","DOIUrl":"10.1111/apha.14245","url":null,"abstract":"<p><strong>Aim: </strong>Calcium-activated ligand-gated chloride channels, beyond their role in maintaining anion homeostasis, modulate neuronal excitability by facilitating nonvesicular neurotransmitter release. BEST1, a key member of this family, is permeable to γ-aminobutyric acid (GABA) and glutamate. While astrocytic BEST1 is well-studied and known to regulate neurotransmitter levels, its distribution and role in other brain cell types remain unclear. This study aimed to reassess the localization of BEST1 in the mouse cerebral cortex.</p><p><strong>Methods: </strong>We examined the localization and distribution of BEST1 in the mouse parietal cortex using light microscopy, confocal double-labeling with markers for astrocytes, neurons, microglia, and oligodendrocyte precursor cells, and 3D reconstruction techniques.</p><p><strong>Results: </strong>In the cerebral cortex, BEST1 is more broadly distributed than previously thought. Neurons are the second most abundant BEST1<sup>+</sup> cell type in the cerebral cortex, following astrocytes. BEST1 is diffusely expressed in neuronal somatic and neuropilar domains and is present at glutamatergic and GABAergic terminals, with a prevalence at GABAergic terminals. We also confirmed that BEST1 is expressed in cortical microglia and identified it in oligodendrocyte precursor cells, albeit to a lesser extent.</p><p><strong>Conclusions: </strong>Together, these findings suggest that BEST1's role in controlling neurotransmission may extend beyond astrocytes to include other brain cells. Understanding BEST1's function in these cells could offer new insights into the molecular mechanisms shaping cortical circuitry. Further research is needed to clarify the diverse roles of BEST1 in both normal and pathophysiological conditions.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14245"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11674994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520406","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}
引用次数: 0
Of manuscripts and memories: Passing the pen to Tobias. 手稿和记忆:把笔交给托拜厄斯。
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-12-19 DOI: 10.1111/apha.14255
Pontus B Persson
{"title":"Of manuscripts and memories: Passing the pen to Tobias.","authors":"Pontus B Persson","doi":"10.1111/apha.14255","DOIUrl":"10.1111/apha.14255","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14255"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142851617","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}
引用次数: 0
Did you know? Is there a reserve in myocardial work via the Frank-Starling mechanism in healthy humans? 您知道吗?健康人通过弗兰克-斯塔林机制进行的心肌工作有储备吗?
IF 5.6 2区 医学
Acta Physiologica Pub Date : 2025-01-01 Epub Date: 2024-09-06 DOI: 10.1111/apha.14230
Meihan Guo, David Montero
{"title":"Did you know? Is there a reserve in myocardial work via the Frank-Starling mechanism in healthy humans?","authors":"Meihan Guo, David Montero","doi":"10.1111/apha.14230","DOIUrl":"10.1111/apha.14230","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":" ","pages":"e14230"},"PeriodicalIF":5.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138685","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}
引用次数: 0
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