ACTA PHYSIOLOGICA 是一个重要论坛，用于发表来自世界各地的作者在生理学和相关领域的高质量原创研究。 ACTA PHYSIOLOGICA 是人类/转化生理学领域的领先期刊，同时促进了生理学科学的各个方面。该杂志发表关于重要的新观察以及评论和评论的完整原创文章。

Acta Physiologica is an important academic forum dedicated to publishing high-quality original research from authors around the world in the fields of physiology and related areas. As a leading journal in human/translational physiology, Acta Physiologica promotes various aspects of physiological science. The journal publishes significant new observations, as well as complete original articles, reviews, and commentaries.

《Acta Physiologica》是一个重要的学术论坛，致力于发表来自全球作者在生理学及相关领域的高质量原创研究。作为人类/转化生理学领域的领先期刊，《Acta Physiologica》促进了生理学科学的各个方面。该杂志发表重要的新观察，以及完整的原创文章、评论和综述。

Acta Physiologica

Abstract Aim Healthy ageing interventions encompass regular exercise to prevent mitochondrial dysfunction, key player in sarcopenia pathogenesis. Mitochondrial biogenesis has been well documented, but mitochondrial remodelling in response to exercise training is poorly understood. Here we investigated fusion, fission and mitophagy before and after an exercise intervention in older adults. Methods Skeletal muscle biopsies were collected from 22 healthy sedentary men and women before and after 4 months of supervised training. Eight lifelong trained age‐ and gender‐matched volunteers served as positive controls. Transmission electron microscopy was used to estimate mitochondrial content. Western blotting and qRT‐PCR were used to detect changes in specific proteins and transcripts. Results After intervention, mitochondrial content increased to levels of controls. While enhancement of fusion was prevalent after intervention, inhibition of fission and increased mitophagy were dominant in controls. Similarly to PARKIN, BCL2L13 content was higher in controls. The observed molecular adaptations paralleled long‐term effects of training on physical fitness, exercise efficiency and oxidative capacity. Conclusions This study describes distinct patterns of molecular adaptations in human skeletal muscle under chronic exercise training. After 16 weeks of exercise, the pattern was dominated by fusion to increase mitochondrial content to the metabolic demands of exercise. In lifelong exercise, the pattern was dominated by mitophagy synchronized with increased fusion and decreased fission, indicating an increased mitochondrial turnover. In addition to these temporally distinct adaptive mechanisms, this study suggests for the first time a specific role of BCL2L13 in chronic exercise that requires constant maintenance of mitochondrial quality.

Yoan Arribat

Nicholas T. Broskey

Chiara Greggio

Marie Boutant

Sonia Conde Alonso

Sameer S. Kulkarni

Sylviane Lagarrigue

Elvis A. Carnero

Cyril Besson

Carles Cantó

Francesca Amati

Acta Physiol

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

Abstract Serotonin or 5‐hydroxytryptamine (5‐ HT ) is a neurotransmitter and hormone that contributes to the regulation of various physiological functions by its actions in the central nervous system ( CNS ) and in the respective organ systems. Peripheral 5‐ HT is predominantly produced by enterochromaffin ( EC ) cells of the gastrointestinal ( GI ) tract. These gut‐resident cells produce much more 5‐ HT than all neuronal and other sources combined, establishing EC cells as the main source of this biogenic amine in the human body. Peripheral 5‐ HT is also a potent immune modulator and affects various immune cells through its receptors and via the recently identified process of serotonylation. Alterations in 5‐ HT signalling have been described in inflammatory conditions of the gut, such as inflammatory bowel disease. The association between 5‐ HT and inflammation, however, is not limited to the gut, as changes in 5‐ HT levels have also been reported in patients with allergic airway inflammation and rheumatoid arthritis. Based on searches for terms such as ‘5‐ HT ’, ‘ EC cell’, ‘immune cells’ and ‘inflammation’ in pubmed.gov as well as by utilizing pertinent reviews, the current review aims to provide an update on the role of 5‐ HT in biological functions with a particular focus on immune activation and inflammation.

M. S. Shajib

W. I. Khan

The role of serotonin and its receptors in activation of immune responses and inflammation

血清素及其受体在激活免疫反应和炎症中的作用

Abstract Chronic kidney disease (CKD) and cardiovascular disease (CVD) have an estimated 700–800 and 523 million cases worldwide, respectively, with CVD being the leading cause of death in CKD patients. The pathophysiological interplay between the heart and kidneys is defined as the cardiorenal syndrome (CRS), in which worsening of kidney function is represented by increased plasma concentrations of uremic toxins (UTs), culminating in dialysis patients. As there is a high incidence of CVD in CKD patients, accompanied by arrhythmias and sudden cardiac death, knowledge on electrophysiological remodeling would be instrumental for understanding the CRS. While the interplay between both organs is clearly of importance in CRS, the involvement of UTs in pro‐arrhythmic remodeling is only poorly investigated, especially regarding the mechanistic background. Currently, the clinical approach against potential arrhythmic events is mainly restricted to symptom treatment, stressing the need for fundamental research on UT in relation to electrophysiology. This review addresses the existing knowledge of UTs and cardiac electrophysiology, and the experimental research gap between fundamental research and clinical research of the CRS. Clinically, mainly absorbents like ibuprofen and AST‐120 are studied, which show limited safe and efficient usability. Experimental research shows disturbances in cardiac electrical activation and conduction after inducing CKD or exposure to UTs, but are scarcely present or focus solely on already well‐investigated UTs. Based on UTs data derived from CKD patient cohort studies, a clinically relevant overview of physiological and pathological UTs concentrations is created. Using this, future experimental research is stimulated to involve electrophysiologically translatable animals, such as rabbits, or in vitro engineered heart tissues.

Willem B. van Ham

Carlijn M. Cornelissen

Toon A. B. van Veen

Uremic toxins in chronic kidney disease highlight a fundamental gap in understanding their detrimental effects on cardiac electrophysiology and arrhythmogenesis

慢性肾脏病中的尿毒症毒素突显了对其对心脏电生理和心律失常有害影响的根本认识差距

In the current issue of Acta Physiologica, Lundberg and co-workers publish a paper entitled "Germ-free mice are not protected against diet-induced obesity and metabolic dysfunction" in which the authors show that feeding a Western diet to both conventionally raised and germ-free mice results in weight gain, increased fat mass, fatty liver, glucose intolerance and adipose tissue inflammation1 . This indicates that development of obesity and components of the metabolic syndrome is not dependent on the presence of gut microbiota and adds to the ongoing discussion regarding the causal role of intestinal microbiota in the development of obesity.

Juergen Eckel

Intestinal microbiota and host metabolism — A complex relationship

肠道微生物群与宿主代谢——一种复杂的关系

Calcitonin gene-related peptide (CGRP) has been viewed as a neuropeptide and vasodilator. However, CGRP is more appropriately thought of as a pleiotropic signalling molecule. Indeed, CGRP has key regulatory functions on immune and inflammatory processes within the skin. CGRP-containing nerves are intimately associated with epidermal Langerhans cells (LCs), and CGRP has profound regulatory effects on Langerhans cell antigen-presenting capability. When LCs are exposed to CGRP in vitro, their ability to present antigen for in vivo priming of naïve mice or elicitation of delayed-type hypersensitivity is inhibited in at least some situations. Administration of CGRP intradermally inhibits acquisition of immunity to Th1-dominant haptens applied to the injected site while augmenting immunity to Th2-dominant haptens, although the cellular targets of activity in these experiments remain unclear. Although CGRP can be a pro-inflammatory agent, several studies have demonstrated that administration of CGRP can inhibit the elicitation of inflammation by inflammatory stimuli in vivo. In this regard, CGRP inhibits the release of certain chemokines by stimulated endothelial cells. This is likely to be physiologically relevant as cutaneous blood vessels are innervated by sensory nerves. Exciting new studies suggest a significant role for CGRP in the pathogenesis of psoriasis and, most strikingly, that CGRP inhibits the ability of LCs to transmit the human immunodeficiency virus 1 to T lymphocytes. A more complete understanding of the role of CGRP in the skin immune system may lead to new and novel approaches for the therapy of immune-mediated skin disorders.

R. D. Granstein

J. A. Wagner

L. L. Stohl

W. Ding

Calcitonin gene‐related peptide: key regulator of cutaneous immunity

降钙素基因相关肽：皮肤免疫的关键调节因子

The stable isotope experiments by Shemin and Rittenberg in the 1940s employed ingested 15N-glycine to determine that red blood cell (RBC) lifespan was approximately 127 days.1 This estimate was much longer than that provided by agglutination methods2 and established the canonical 120-day lifespan for RBCs that appears in all textbooks today. While this finding is fundamental to our understanding of erythropoiesis in humans, the 15N-glycine method, like other cell labeling methods, models the decay in tracer abundance to estimate the average lifespan of RBCs, which requires an extended protocol (~5–6 months). While a fractional synthetic rate can be estimated from the lifespan (e.g., 120 days corresponds to a turnover rate of 0.8%/day), a more direct and rapid method to assess the rate at which RBCs are produced would be more practical and advantageous for research questions involving interventions. Characteristics of hemoglobin (Hb)—slow turnover and accessibility—make it feasible to assess its fractional synthetic rate with the deuterated water (2H2O) oral stable isotope method (Figure 1).3 Given that Hb comprises ~97% of all RBC protein,4 its synthesis rate is a surrogate of RBC production. While experiments with 2H2O by Ussing in 1941 indicated that this technique had potential in rodents, it was not developed further or applied to human research.5 After dosing with 2H2O, the Hb fractional synthetic rate can theoretically be measured when a linear increase in alanine-bound 2H isolated from Hb is observed in conjunction with stable 2H enrichment in the precursor pool. Although the precursor pool (i.e., bone marrow) is difficult to access in humans, measuring body water 2H enrichment is a noninvasive and valid surrogate.6 As almost all of the proteins in RBCs are synthesized during maturation in the bone marrow,7 there is a delay between the synthesis of Hb and its appearance in the blood. This process requires an extended protocol compared to the use of 2H2O in skeletal muscle (i.e., weeks vs. days), but it is possible to account for this delay in calculations of the fractional synthetic rate. Furthermore, because the total mass of Hb in circulation (i.e., hemoglobin mass or Hbmass) can be measured in humans,8 it is also theoretically possible to measure the absolute synthetic rate for Hb as well as fractional and absolute breakdown rates for Hb. Given the much shorter duration and relative simplicity of the protocol, this oral stable isotope method to measure Hb synthesis could provide insights into many areas of human physiology (e.g., exercise, environmental, clinical). Furthermore, this technique could improve diagnoses and treatments for conditions such as hemolytic anemia or chronic kidney disease through investigations of the underlying pathologies, measures of patient-specific RBC lifespan, or assessments of erythropoietic responses to treatments. As part of a larger study approved by the University of Calgary Conjoint Health Research Ethics Board (REB19-0215)—and conforming to the standards set by the Declaration of Helsinki, except for registration in a database—we assessed the fractional synthetic rate for Hb in humans. Representative data for one participant (female, 28 years) is reported. Using the 2H2O method, the Hb fractional synthetic rate for this individual was 0.78%/day, translating to a Hb lifespan of ~128 days, and an absolute synthetic rate of 5.3 g/day, given a Hbmass of 671 g. While the 2H2O method appears to be useful for quantifying Hb synthesis and could facilitate future studies in human physiology related to erythropoiesis, some assumptions used to calculate protein synthesis rates from metabolic tracer data must be clarified. First, we need to measure APE in the correct precursor pool. Since the measurement period in the present study was weeks rather than hours, it is almost certain that the 2H-labeled free alanine pool present in bone marrow was in equilibrium with 2H-labeled body water and therefore this assumption can be considered met. Second, we need to measure APE in the correct protein of interest. As 97% of RBC protein is Hb,4 we analyzed proteins liberated from the RBC fraction of blood samples without further Hb-isolating methods. Third, we must assume that no recycling of the precursor takes place. While ineffective erythropoiesis,11 the destruction of developing RBC in the marrow, can be significant in disorders of hemoglobin synthesis (e.g., folate or iron deficiency or thalassemia), our representative participant had no known conditions affecting erythropoiesis, meaning this process is unlikely to be a major factor contributing to precursor recycling. While significant shedding of Hb-containing vesicles from circulating RBCs is possible, it is unlikely to impact the 2H2O method, given this phenomenon seemingly occurs in the second half of the RBC lifecycle (i.e., after 60 days of age).12 Finally, because there is a delay in the appearance of labeled Hb relative to synthesis (Figure 1), the precursor and protein enrichments need to be aligned for calculation. Given that it took ~2 weeks for 2H label appearance in Hb to stabilize, we chose to use the body water APE from 2 weeks prior (i.e., first 14 days) when calculating the fractional synthetic rate for Hb using the final 14 days. As body water enrichment was relatively stable (Figure 1), this decision only had a minor effect on our calculations. In conclusion, the novel method to quantify the Hb synthetic rate by deuterated water labeling is feasible and provides results aligning with expected rates of erythropoiesis, previously only indirectly derived from RBC lifespan measurements. Future studies can use the technique to investigate the erythropoietic process in various clinical conditions or in response to exercise, nutritional, and environmental stressors, and for cross-validation of existing techniques in hematology. Hilkka Kontro: Conceptualization; investigation; writing – original draft; methodology; visualization; writing – review and editing; formal analysis; data curation. Chris McGlory: Conceptualization; investigation; methodology; visualization; writing – review and editing; formal analysis; resources; supervision; project administration. Martin J. MacInnis: Conceptualization; investigation; funding acquisition; writing – original draft; methodology; visualization; writing – review and editing; formal analysis; project administration; supervision; resources; data curation. The authors would like to thank the participants as well as Oluwatimilehin Ajayi for his help with data collection. This work was supported by an operating grant from the Natural Sciences and Engineering Research Council of Canada (NSERC; grant number RGPIN-2018-06424), start-up funding from the Faculty of Kinesiology (University of Calgary), and a University of Calgary VPR Catalyst Grant, all received by MJM. HK was supported by a Faculty of Kinesiology Dean's Doctoral Scholarship. The data that support the findings of this study are available from the corresponding author upon reasonable request.

Hilkka Kontro

Chris McGlory

Martin J. MacInnis

Deuterated water (<scp>2H2O</scp>) can be used to quantify hemoglobin synthesis and red blood cell lifespan in humans

重水（<scp>2H2O</scp>）可用于量化人体血红蛋白合成和红细胞寿命

Imagine awarding authors one of the highest honors in scientific publishing, only to receive an insult in response. Picture writing to inform them they've won the US$100000 Acta Physiologica Award, and instead of gratitude, getting a fiery phone call. Initially, the author thought it was a prank. But once the truth sunk in, it was amusing to witness the quick change in tone—scrambling to recover and secure the award. Reflecting on 12 years as Editor-in-Chief of Acta Physiologica, the predominant feeling is one of the deep gratitude and pride. The long journey transformed the journal, elevating its readership, recognition, and scientific impact to new heights. This success is due to the unwavering dedication of our authors, the expertise of our reviewers, the editorial team's rigor, and the enthusiasm of our readers. Together, we've shaped Acta Physiologica into an internationally respected journal that pushes the field of physiology ever forward. Today, the editorial team and I are thrilled to welcome Professor Tobias Wang as the new Editor-in-Chief. A distinguished physiologist from Aarhus University, Tobias brings a remarkable depth of experience and an impressive record of achievements. His pioneering work in respiratory and comparative physiology, along with his insights into thermoregulation, make the foremost voice in the field, as seen in his acclaimed articles and television appearances. Having collaborated with Tobias on our editorial team, it's clear he has the vision and drive to lead Acta Physiologica to even greater success. He is the force behind our journal's latest developments. We are all in great debt to our previous expert editors Joakim Ek, Lena Eliasson, Karl-Heinz Herzig, Tadashi Isa, Sari Lauri, Bridgit Lumb, Mikko Nikinmaa, Mia Phillipson, and Ursula Seidler. Naturally, the true Chief Editor of this term, Carola Neubert is unforgotten. Inside the eye of the tornado, she makes order out of chaos and will stay onboard with Tobias. Excuse me Peter (Peter Bie) for being such a pain in the neck at times. You are the one I thank most for providing me with the honor of becoming Acta Physiologica's Chief Editor and you are the one that bailed me out when my visions got out of hand. Besides that, you were the first expert editor for kidney physiology during my term and a great friend. Together, these extraordinary scientists have shaped Acta Physiologica to reflect the very best of physiology across its diverse fields. Alongside our broader community of readers and contributors, they have transformed the journal over the past decade. As the official journal of the Scandinavian Physiological Society (SPS), Acta Physiologica fulfills a unique mission. The SPS, a charitable nonprofit, reinvests journal profits back into the physiological community—funding travel grants, symposia, awards, and more. Being part of a journal that prioritizes the growth of physiologists worldwide, fostering international collaboration, and advancing new research feels profoundly rewarding. I cannot step away from this role without extending heartfelt thanks to the SPS for their trust and to our entire editorial board for their constant support and guidance. Acta Physiologica owes much to the generous contributions of past Editors, particularly Jan Henriksson, who elevated the journal to new levels of excellence and mentored me as Börje Üvnas mentored him. Carrying forward their legacy has been humbling and deeply rewarding. My years with Acta Physiologica have been an unforgettable honor, filled with moments of challenge, excitement, and profound satisfaction. Knowing the journal is in capable hands with Tobias Wang only makes this transition more thrilling. Tobias's vision and dedication will propel Acta Physiologica to new heights, and I look forward to supporting him and the SPS however I can in the years ahead. Thank you all for a remarkable 12 years. In particular to Anja, my wife (Figure 1) for her ExActas and for Magnus. You two make life worthwhile. While Acta Physiologica's impact factor reaches for the stars, the outgoings Editor's impact factor was always two (left: Anja, right: Magnus). Always keep in mind Tobias: H-indexes and impact factors fluctuate, while the metrics of life keeps us going. Here's to the future of Acta Physiologica. Deeply touched, Pontus. The author is fully biased with regard to the SPS in general, and Acta Physiologica in particular.

Pontus B. Persson

Of manuscripts and memories: Passing the pen to Tobias

手稿与记忆：将笔交给托比亚斯

Rodney and colleagues provide compelling evidence for the therapeutic potential of selective histone deacetylase 6 (HDAC6) inhibition in mdx mice, a widely used model of Duchenne muscular dystrophy (DMD).1 Their study reveals that HDAC6 inhibition promotes enhanced autophagy through increased tubulin acetylation, offering new hope for treatment strategies targeting this critical enzyme. This research sheds light on the potential of HDAC6 inhibitors to address some of the key pathological features of DMD. Duchenne muscular dystrophy is a severe, progressive neuromuscular disorder caused by mutations in the dystrophin gene on the X chromosome.2 Affecting approximately 1 in 3500 male births, DMD leads to the absence of dystrophin, a structural protein that connects muscle fibers to the extracellular matrix. Without dystrophin, muscle cells are vulnerable to damage and progressive degeneration. DMD typically presents in early childhood, with delayed motor milestones, muscle weakness, and difficulty standing. As the disease progresses, children develop a characteristic waddling gait, difficulty climbing stairs, and progressive muscle loss, ultimately leading to wheelchair dependence by age 12. Complications such as skeletal deformities, breathing difficulties, and cardiomyopathy arise, and most patients do not survive beyond their 30s due to respiratory and cardiac failure. Despite two decades of research, no cure for DMD exists, and current treatments remain limited to glucocorticoid therapy. Although innovative genetic approaches, such as exon skipping, gene editing with CRISPR/Cas9, and viral vector-mediated dystrophin delivery, show promise, challenges like inconsistent efficacy, off-target effects, and incomplete dystrophin restoration in muscle tissues—especially in the heart—have slowed progress. As a result, a more comprehensive treatment strategy, combining genetic and pharmacological approaches, is likely necessary to address the multifaceted nature of DMD. Over the past 20 years, HDAC inhibitors have shown promise in pre-clinical DMD models. Givinostat, a pan-HDAC inhibitor, was recently FDA-approved for its ability to slow disease progression in ambulatory boys with DMD.3 However, pan-HDAC inhibitors can have undesirable side effects, including genotoxicity and impaired DNA repair. To mitigate these risks, more selective HDAC inhibitors have been developed, with HDAC6 emerging as a particularly attractive target. HDAC6-specific inhibitors have been shown to have several advantages over pan-HDAC inhibitors, including a lack of severe side effects. For instance, HDAC6 knockout mice do not exhibit significant pathological features, suggesting that selective inhibition of HDAC6 may be safe and beneficial.4 In animal models, HDAC6 inhibition has demonstrated therapeutic effects in a range of disorders, including cancer, neurodegenerative diseases, and cardiomyopathies, without notable adverse outcomes.5 In the context of neuromuscular diseases like Charcot–Marie–Tooth disease and Amyotrophic Lateral Sclerosis (ALS), HDAC6 inhibition has been shown to reverse axonal loss, promote muscle reinnervation, and improve survival. In muscular dystrophies, HDAC6 inhibition has been linked to improvements in muscle strength, reduced inflammation and fibrosis, and the partial restoration of the dystrophin-glycoprotein complex and neuromuscular junctions.6 These effects are thought to arise from HDAC6-mediated stabilization of microtubules and inhibition of TGF-β signaling respectively due to the inhibition of Smad3 and tubulin deacetylation, both of which are key pathways in muscle regeneration.7 One of the key findings of Rodney et al.'s study is the role of autophagy in DMD muscle pathology. In mdx mice and DMD patients, autophagic processes are impaired, leading to an accumulation of damaged cellular components.8 The study shows that HDAC6 inhibition restores autophagic function by promoting microtubule acetylation. This process is critical for the proper maturation of autophagosomes, the vesicles that digest and recycle cellular debris.9 Specifically, the study highlights two key defects in mdx muscles: impaired vesicle nucleation and phagophore elongation during the early stages of autophagy, as well as compromised fusion of autophagosomes with lysosomes in the later stages. HDAC6 inhibition, particularly through the use of tubastatin A—a selective HDAC6 inhibitor—was shown to reverse these defects, restoring both early and late stages of autophagy in dystrophic muscle cells. The authors further explore the interplay between acetylation and redox regulation in autophagy. In mdx muscles, increased Nox2 activity disrupts autophagy through the mTOR pathway and microtubule dynamics.10 However, while Nox2 inhibition preserves the microtubule network, it does not restore autophagosome-lysosome fusion or acetylation, indicating that microtubule acetylation is a critical factor in the fusion process. This finding underscores the importance of acetylation in maintaining autophagic function in DMD muscles (Figure 1). Rodney and colleagues' study significantly advances our understanding of the mechanisms underlying HDAC6 inhibition's beneficial effects in DMD. By demonstrating that HDAC6 inhibition restores autophagy and promotes muscle recovery, their work paves the way for the development of targeted therapies aimed at modulating autophagic pathways in DMD. Further research will be needed to explore the specific molecular targets of HDAC6, including potential effects on other proteins involved in the autophagic process, and to evaluate the long-term safety and efficacy of HDAC6 inhibitors in clinical settings. In conclusion, this study highlights the therapeutic potential of HDAC6 inhibition in DMD, offering a promising avenue for further exploration. By addressing critical cellular processes like autophagy, these inhibitors may provide a much-needed complement to existing DMD treatments, helping to slow disease progression and improve the quality of life for affected individuals. Alexis Osseni: Conceptualization; writing – original draft; writing – review and editing; funding acquisition. Laurent Schaeffer: Conceptualization; writing – original draft; writing – review and editing; funding acquisition. The author acknowledges the use of ChatGPT to edit the text to improve its form. Funding for this work was obtained via a grant from the Association Française contre les Myopathies (AFM-Téléthon) through strategic MyoNeurALP1 & MyoNeurALP2 alliances. Additional support for this work came from the Fondation Médicale pour la Recherche (FMR) and the Fondation Maladies Rares. The authors declare no conflict of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request.

Alexis Osseni

Laurent Schaeffer

Targeting histone deacetylase 6 (<scp>HDAC6</scp>) in Duchenne muscular dystrophy: New insights into therapeutic potential

靶向组蛋白去乙酰化酶6（HDAC6）在杜氏肌营养不良中的作用：治疗潜力的新见解

Onesmo B. Balemba

Brian D. Gulbransen

Acta Physiol (Oxf)

A potential link between enteric glia and the pathophysiology of diet‐induced obesity and related metabolic diseases

肠道胶质细胞与饮食诱导的肥胖及相关代谢疾病病理生理学之间的潜在联系

Abbreviation	Acta Physiol
Journal Impact	5.44
Quartiles(Global)	PHYSIOLOGY(Q1)

ISSN	1748-1708, 1748-1716
h-index	133

Publication Information	Publisher: John Wiley and Sons Ltd，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2006，Proportion of original research papers: 71.79%，Self Citation Rate:25.00%， Gold OA Rate: 45.49%
Average review cycle	网友分享经验：偏慢,4-8周
Average recruitment ratio	网友分享经验：较易

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Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

The role of serotonin and its receptors in activation of immune responses and inflammation

Uremic toxins in chronic kidney disease highlight a fundamental gap in understanding their detrimental effects on cardiac electrophysiology and arrhythmogenesis

Intestinal microbiota and host metabolism — A complex relationship

Calcitonin gene‐related peptide: key regulator of cutaneous immunity

Deuterated water (²H₂O) can be used to quantify hemoglobin synthesis and red blood cell lifespan in humans

Of manuscripts and memories: Passing the pen to Tobias

Targeting histone deacetylase 6 (HDAC6) in Duchenne muscular dystrophy: New insights into therapeutic potential

A potential link between enteric glia and the pathophysiology of diet‐induced obesity and related metabolic diseases

Did you know: Kangaroos are resistant to ventricular arrhythmia

Acta Physiologica

Journal Citation Format

A journal article with 1 author

A journal article with 2 authors

A journal article with 3 authors

A journal article with 5 or more authors

Books Citation Format

Thesis Citation Format

Web sites Citation Format

Patent Citation Format

Staying up late manually editing references? ivySCI automatically matches journals and helps you generate references with a single click.

Share Submission Experience

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

The role of serotonin and its receptors in activation of immune responses and inflammation

Uremic toxins in chronic kidney disease highlight a fundamental gap in understanding their detrimental effects on cardiac electrophysiology and arrhythmogenesis

Intestinal microbiota and host metabolism — A complex relationship

Calcitonin gene‐related peptide: key regulator of cutaneous immunity

Deuterated water (2H2O) can be used to quantify hemoglobin synthesis and red blood cell lifespan in humans

Of manuscripts and memories: Passing the pen to Tobias

Targeting histone deacetylase 6 (HDAC6) in Duchenne muscular dystrophy: New insights into therapeutic potential

A potential link between enteric glia and the pathophysiology of diet‐induced obesity and related metabolic diseases

Did you know: Kangaroos are resistant to ventricular arrhythmia

Deuterated water (²H₂O) can be used to quantify hemoglobin synthesis and red blood cell lifespan in humans