Acta Physiologica最新文献

{"title":"Role of the Choroid Plexus Kir7.1 Channel in the Regulation of Mouse Cerebrospinal Fluid K+ Concentration","authors":"Juan Carlos Henao,&nbsp;Johanna Burgos,&nbsp;Erwin Vera,&nbsp;Iván Ruminot,&nbsp;L. Pablo Cid,&nbsp;Isabel Cornejo,&nbsp;Francisco V. Sepúlveda","doi":"10.1111/apha.70129","DOIUrl":"10.1111/apha.70129","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>K⁺ channel Kir7.1 is prominently expressed at the apical membrane of the choroid plexus epithelium (CPE) together with the Na⁺-K⁺-ATPase pump and cotransporter NKCC1. Its unusual independence of extracellular K⁺ ([K⁺]_o) suggests a key role in regulating cerebrospinal fluid (CSF) K⁺ concentration ([K⁺]_CSF). We tested this hypothesis by exploring the effect of Kir7.1 inactivation or modification of its K⁺-dependence in mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We generate conditional Kir7.1 knockout (cKO) and knockin mice carrying the M125R mutation altering Kir7.1 K⁺-dependence. We study the electrical properties of CPE cells in vitro as well as in vivo CSF secretion and [K⁺]_CSF. CPE NKCC1 activity, expression and phosphorylation status were also evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Kir7.1 identified as the primary [K⁺]_o-independent conductance in CPE cells, critically contributes to their membrane potential. CPE cells from Kir7.1-M125R mice exhibited a K⁺ conductance with direct dependence on [K⁺]_o. While CSF secretion rates were unaltered in both cKO Kir7.1 and M125R animals, [K⁺]_CSF was significantly decreased in cKO mice and increased in M125R mutants. Unexpectedly, NKCC1 activity was strongly inhibited in Kir7.1 cKO CPE despite unaltered expression and phosphorylation levels, but remained unaffected in M125R cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Kir7.1 imparts high K⁺ permeability and defines the membrane potential of CPE cells. Its unusual [K⁺]_o-independent conductance underpins its important role in the regulation of [K⁺]_CSF. Moreover, Kir7.1 appears crucial for NKCC1 function, likely these two proteins forming part of an apical complex with the Na⁺-K⁺-ATPase. Given the continuity of CSF with brain interstitial space, Kir7.1-mediated control of [K⁺]_CSF might influence neuronal excitability.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145487165","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":"Unique Role of Proximal Tubule Dipeptidyl Peptidase 4 on Blood Pressure, Renal Sodium Handling, and Na+/H+ Exchanger Isoform 3 Phosphorylation","authors":"Flavia L. Martins,&nbsp;Joao Carlos Ribeiro-Silva,&nbsp;Erika Fernandes de Jesus,&nbsp;Ravi Nistala,&nbsp;Adriana C. C. Girardi","doi":"10.1111/apha.70127","DOIUrl":"10.1111/apha.70127","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Dipeptidyl peptidase 4 (DPP4) is a transmembrane serine exopeptidase highly expressed in the proximal tubule (PT). While its enzymatic role is well characterized, its non-enzymatic functions remain unclear. DPP4 physically associates with the Na⁺/H⁺ exchanger isoform 3 (NHE3), and DPP4 inhibitors promote natriuresis; however, the mechanisms by which DPP4 regulates NHE3 and its role in blood pressure (BP) regulation remain controversial. We hypothesized that PT DPP4 promotes sodium reabsorption and attenuates pressure–natriuresis by preventing NHE3 phosphorylation at serine 552 (pS552).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We generated PT-specific <i>Dpp4</i> knockout mice (<i>Dpp4</i>^ΔPT) and examined the effects of PT-specific and global <i>Dpp4</i> deletion (<i>Dpp4</i>^−/−) on systolic blood pressure (SBP), natriuresis, and NHE3 phosphorylation at baseline and following acute angiotensin II (Ang II) infusion in male and female mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Both <i>Dpp4</i>^ΔPT and <i>Dpp4</i>^−/− showed enhanced diuretic and natriuretic responses to saline loading, with higher renal pS552-NHE3, and unchanged baseline SBP. Ang II elevated DPP4 activity in controls but not in <i>Dpp4</i>^ΔPT mice, suggesting that PT DPP4, rather than DPP4 in other nephron segments, is regulated by Ang II under these experimental conditions. Ang II increased SBP in all groups, but the pressor response was significantly attenuated in both <i>Dpp4</i>^ΔPT and <i>Dpp4</i>^−/− mice, paralleling sustained pS552-NHE3 elevation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings demonstrate that DPP4 modulates NHE3 activity by preventing pS552-NHE3 accumulation, promoting an anti-natriuretic effect. In the absence of PT DPP4, these mechanisms are disrupted, reducing Ang II sensitivity, maintaining high pS552-NHE3 levels, and likely enhancing pressure–natriuresis, underscoring the role of PT DPP4 in modulating signaling mechanisms governing renal function.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145443537","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":"Mechanisms That Prevent Vascular Leakage During Leukocyte Extravasation","authors":"Siem J. de Haan,&nbsp;Jaap D. van Buul","doi":"10.1111/apha.70126","DOIUrl":"10.1111/apha.70126","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Inflammation is the response of the immune system against harmful stimuli in tissues. Leukocyte extravasation or TransEndothelial Migration (TEM) is a crucial step during inflammation, in which leukocytes migrate over the endothelial barrier toward the damaged tissue.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Historically, it was believed that leukocyte TEM directly causes excessive vascular leakage, resulting in tissue edema. However, it is now clear that leukocyte TEM and vascular leakage are uncoupled events with different spatiotemporal regulation. Moreover, several mechanisms have been identified that prevent vascular leakage during leukocyte TEM.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Here we summarize the different mechanisms that are responsible for limiting the leakage during the transmigration event and explore their clinical relevance in developing targeted therapeutics for controlling vascular leakage in inflammatory diseases.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12579809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145426390","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":"Mitochondrial Dysfunction Contributes to Decompensation in a Zebrafish Model of Isoproterenol-Induced Heart Failure","authors":"Manuel Vicente,&nbsp;Aaron García-Blázquez,&nbsp;Antonio Martínez-Sielva,&nbsp;Jussep Salgado-Almario,&nbsp;Joaquín Jordán,&nbsp;Beatriz Domingo,&nbsp;Juan Llopis","doi":"10.1111/apha.70128","DOIUrl":"https://doi.org/10.1111/apha.70128","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Heart failure is a clinical syndrome where the heart's structural or functional impairment leads to inadequate blood flow to meet the body's metabolic demands. Mitochondrial dysfunction is increasingly recognized as a central contributor underlying the contractile impairment observed in the failing heart. This study aimed to explore the interplay between calcium dynamics, cardiac mechanical performance, and mitochondrial ATP production during the progression of heart failure in zebrafish larvae exposed to chronic isoproterenol stimulation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Heart failure was induced by treating zebrafish larvae with 100 μM isoproterenol from 3 to 14 days postfertilization (dpf). Cardiac calcium transients, contractility, and mitochondrial ATP levels were assessed in vivo using transgenic lines expressing specific fluorescent biosensors. Additionally, transcriptomic analysis by RNA sequencing was performed on hearts collected at 14 dpf following prolonged isoproterenol exposure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>After 4 days of isoproterenol treatment (7 dpf), larvae exhibited ventricular dilation, reduced calcium levels, and diminished contractile force (<i>p</i> &lt; 0.0001), although cardiac output remained intact. In contrast, extended treatment (11 days; 14 dpf) led to decompensated heart failure, characterized by a significant decline in cardiac output (<i>p</i> &lt; 0.0001). Mitochondrial ATP levels were preserved at 7 dpf but dropped markedly at 14 dpf (<i>p</i> &lt; 0.0001). Transcriptomic profiling at this later stage revealed downregulation of key functions (<i>p</i> &lt; 0.05) involved in mitochondrial energy metabolism and energy transfer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In this model, heart dysfunction was initially evidenced by cardiac dilation. At 4 days of isoproterenol treatment, calcium levels and contractility decreased. Subsequently, decompensation coincided with a collapse in mitochondrial ATP production.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145407314","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":"Estrogen and Estrogen Receptors in Cardioimmunology: Implications in Physiology, Pathophysiology, and Therapeutic Strategies","authors":"Hongjian Hou,&nbsp;Gabriel K. Adzika","doi":"10.1111/apha.70124","DOIUrl":"10.1111/apha.70124","url":null,"abstract":"<div>\u0000 \u0000 <p>Estrogen (E2) and estrogen receptors (ERs) play vital roles in conferring cardioprotection by modulating several immunological homeostatic responses in cardiovascular tissues. Over the recent decades, the role of inflammatory responses as a tangential component impacting cardiac function and disease are being appreciated and investigated to elucidate the underlying pathomechanisms, identify and develop therapeutic strategies; thus, the emergence of the multi-disciplinary field—cardioimmunology. Here, after summarizing expressions and functionalities of ERs in cellular constituents of the cardiovascular system, we discuss synergistic estrogenic signaling mechanisms preserving cardiovascular function and immune homeostasis. Next, we review studies implicating E2 and ERs in inflammation-driven cardiovascular disease initiation and progression and highlight therapeutic strategies and clinical implications to foster further research into promoting cardiovascular health.</p>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399137","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":"Caloric Restriction Substantially Improves Glucose Regulation in Mice With Hnf1a-Deficient Beta-Cells","authors":"Shayla Sharmine,&nbsp;Thomas Aga Legøy,&nbsp;Lucas Unger,&nbsp;Joao A. Paulo,&nbsp;Luiza Ghila,&nbsp;Simona Chera","doi":"10.1111/apha.70121","DOIUrl":"10.1111/apha.70121","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>HNF1A-MODY, the most prevalent form of monogenic diabetes, displays incomplete penetrance, indicating the involvement of other environmental and genetic factors in the disease etiology. Currently, it is largely unknown what the influence of environmental factors, such as toxins or diet, is on HNF1A-MODY onset and progression. Here we address this issue by exploring the impact of diet on islet and insulin-secreting beta-cells in the context of HNF1A mutation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Transgenic mice allowing the specific Hnf1a mutation in insulin-secreting beta-cells were exposed to four distinct dietary regimens including combinations of high-fat diet and caloric restriction. In vitro stem cell islets bearing the HNF1A^P291fsinsC heterozygous mutation and their isogenic controls were used for validation in humans. The readouts included physiological tests, immunofluorescence, proteomics, bulk, and single-cell transcriptomics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Hnf1a-deficient beta-cells exhibited high sensitivity to dietary cues. Exposure to a high-fat diet exacerbated the glucose regulation defects, while caloric restriction significantly improved blood glucose levels in vivo, without perturbing islet architecture. The high-throughput methods identified changes in the Hnf1a-deficient beta-cells proteome landscape, involving conserved critical regulators of metabolic and growth processes, such as the Carbohydrate Response Element Binding Protein (Chrebp/Mlxipl) and ATP citrate lyase (Acly) among others.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study hallmarks the important impact of diet on Hnf1a-deficient beta-cells, stemming new therapeutic perspectives, such as future diet management approaches.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399151","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":"Immunological Protein Signature During Acute Exercise","authors":"Charlotte Wenzel,&nbsp;David Walzik,&nbsp;Tiffany Wences,&nbsp;Sina Trebing,&nbsp;Klaus Meyer,&nbsp;Andreas Groll,&nbsp;Philipp Zimmer,&nbsp;Niklas Joisten","doi":"10.1111/apha.70125","DOIUrl":"10.1111/apha.70125","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399170","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":"Exploring Desmin as a Potential Modifier in Duchenne Muscular Dystrophy–Associated Cardiomyopathy","authors":"Brice-Emmanuel Guennec,&nbsp;Yeranuhi Hovhannisyan,&nbsp;Gaëlle Revet,&nbsp;Sila Polat,&nbsp;Medhi Hassani,&nbsp;Nathalie Mougenot,&nbsp;Inès Barthelemy,&nbsp;Stephane Blot,&nbsp;Caroline Cieniewski-Bernard,&nbsp;Arnaud Ferry,&nbsp;Ekaterini Kordeli,&nbsp;Zhenlin Li,&nbsp;Onnik Agbulut","doi":"10.1111/apha.70117","DOIUrl":"10.1111/apha.70117","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Duchenne muscular dystrophy (DMD), a rare X-linked genetic disorder, is affecting skeletal and cardiac muscles due to the loss of the dystrophin protein. Modifier proteins, whose expression is altered in DMD patients, may influence disease progression. Desmin, a muscle-specific intermediate filament protein, is increased in the skeletal muscle of mdx mice, a murine model of DMD with a mild phenotype. Here, we inquired whether desmin acts as a modifier in DMD-associated cardiomyopathy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Soluble and insoluble desmin levels were quantified in the hearts of two mdx mouse models (B10.mdx and D2.mdx), and GRMD dystrophic dogs. The expression of desmin-regulatory proteins was also assessed in mdx mice. To assess the impact of desmin levels on the phenotype, we generated mdx mice either desmin-deficient (mdx-Des^−/−) or with reduced levels of desmin by introducing a heterozygous desmin knock-out allele (mdx-Des^+/−). Phenotypic analyses included cardiac function assessment and histological evaluation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In mdx mice, desmin was elevated in its insoluble, phosphorylated, and presumably filamentous form, while GRMD dogs with a severe DMD-like phenotype showed no such increase. Desmin deficiency in mdx mice led to severely aggravated dystrophic features, including cardiac dysfunction and increased fibrosis. Moreover, partial desmin reduction in mdx-Des^+/− mice led to the abrogation of insoluble desmin increase and worsened the mild mdx dystrophic phenotype.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Increased filamentous desmin appears to be protective in mdx mouse hearts and may modulate the severity of DMD cardiomyopathy. These findings support a modifier role for desmin and highlight this protein as a potential therapeutic target for DMD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70117","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399162","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":"Is Predisposition to T2D Impacted by Polymorphisms in Genes Involved in Insulin Signaling and Cellular Bioenergetics?","authors":"Benudhara Pati,&nbsp;Martin Jastroch,&nbsp;Naresh Chandra Bal","doi":"10.1111/apha.70122","DOIUrl":"10.1111/apha.70122","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Type 2 diabetes (T2D) represents a growing global health challenge, with its prevalence and associated metabolic complications rising sharply over the past two decades. Although the pathogenesis of T2D is complex and influenced by lifestyle and (micro)environmental factors, genetic constituents have been considered major predisposing factors. Recent literature shows significant individual variations in both the progression of T2D and the efficacy of antidiabetic drugs. These individual variations are expected to emanate from the inherent genetic make-up and potential epigenetic modifications by environmental factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Hypothesis</h3>\u0000 \u0000 <p>It has been proposed that altered metabolism (including cellular bioenergetic mechanisms) provides protection from T2D. Moreover, several researchers have proposed that proteins regulating cellular bioenergetics, for example, involved in adaptive thermogenesis, represent good targets to counter T2D. Therefore, we thoroughly searched the literature on genetic variability associated with T2D in this review.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We could only find genes involved in (1) insulin secretion (<i>INS</i>, <i>PDX1</i>, <i>ABCC8</i>, <i>KCNJ11</i>, <i>KCNQ1</i>, <i>CDKAL1</i>, <i>IGFBP2</i>) and (2) cellular bioenergetics in insulin-responsive tissues (<i>INSR</i>, <i>IRS</i>, <i>AKT</i>, <i>SLC2A4</i>, <i>TBC1D4</i>, <i>PPP1R3A</i>, <i>LEP</i>, <i>LEPR</i>, <i>ADIPOQ</i>, <i>TCF7L2</i>, <i>PPAR-γ</i>, <i>SLC30A8</i>). Specific attention is given to diverse ethnic populations, in particular Indian subgroups where these genetic factors may display clearer association to T2D.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>By emphasizing genetic predispositions, this review highlights the lack of studies on the genetic association of cellular bioenergetics proteins in T2D pathogenesis. It also underscores the potential for early detection, personalized management, and the development of targeted therapies for individuals with T2D across different genetic profiles.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"241 12","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399207","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":"Twenty-Four Hour Rhythms in Cardiovascular Physiology","authors":"Morten B. Thomsen","doi":"10.1111/apha.70116","DOIUrl":"10.1111/apha.70116","url":null,"abstract":"<p>Many physiological parameters, such as heart rate and blood pressure, display pronounced daily rhythms, with significant differences between day and night levels. The ability to anticipate the 24 h cycle of ambient light confers an adaptive advantage, allowing organisms to prepare for periods of activity and rest. Considering chronophysiology is essential when designing, conducting, and interpreting laboratory experiments because of the often considerable amplitude of the rhythms. This review introduces a straightforward mathematical tool to detect 24 h rhythms in physiological datasets. Next, the review examines 24-h diurnal rhythms in heart rate, QT interval, and blood pressure, based on telemetry recordings from conscious, freely moving mice. These examples illustrate how long-term, continuous monitoring of physiological parameters enables precise characterization of daily cycles when present. Furthermore, the large datasets obtained through methods such as telemetry make it possible to determine whether the observed rhythms are dependent on heart rate. Circadian and diurnal rhythms play an essential role in cardiovascular physiology, influencing key parameters such as heart rate and blood pressure. Considering chronophysiology is therefore essential when designing, conducting, and interpreting physiological studies.</p>","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.70116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145306395","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}