PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY普弗吕格生理学档案——欧洲生理学杂志
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY(英文缩写 PFLUG ARCH EUR J PHY),ISSN 0031-6768,eISSN 1432-2013,中文译名:普弗吕格生理学档案——欧洲生理学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.458 | Q2 |
| 2022 | 4.500 | Q1 |
| 2023 | 2.900 | Q2 |
| 2024 | 2.900 | Q2 |
| 2025 | 3.200 | Q2 |
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY 最新收录文献
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1. NS1643 enhances the activity of T1019PfsX38 and Q1070X hERG channels associated with long QT syndrome type 2.
PMID:日期:2026-10-02Type 2 long QT syndrome (LQT2) increases the risk of cardiac arrest and sudden death due to reduced rapid delayed rectifier potassium currents (IKr) in the heart. Caused by loss-of-function genetic variants in the hERG K channel, LQT2 might benefit from variant-targeted therapy approaches. T1019PfsX38 and Q1070X are LQT2-causing variants reported in Oman and Saudi Arabia. Although nonsense-mediated mRNA decay (NMD) has been proposed to contribute to reduced expression of these truncating variants, it remains unclear whether residual mutant hERG channel function can be pharmacologically enhanced. We used the patch-clamp technique and examined the effects of the hERG potentiator NS1643 on wild-type-, T1019PfsX38- and Q1070X-hERG channels expressed in HEK293 cells. We started by assessing the response of these variants under the influence of a ventricular action potential clamp protocol, then used additional protocols to elucidate the drug's mechanism of action. NS1643 [10 µM] enhanced the repolarization currents in wild-type-, T1019PfsX38- and Q1070X-expressing cells. Its effect was associated with accelerated activation rates and a negative shift in the voltage dependence of activation. In addition, NS1643 suppressed fast deactivation transitions. We conclude that the functions of T1019PfsX38- and Q1070X-hERG channels can be augmented by hERG potentiators if NMD is incomplete, which may facilitate the development of a mechanism-based rescue approach.
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2. Analysis of sodium self-inhibition of the epithelial sodium channel (ENaC) using classical and medium-throughput automated two-electrode voltage-clamp recordings.
PMID:日期:2026-09-28The epithelial sodium channel (ENaC) is a key regulator of electrolyte homeostasis and blood pressure. A characteristic ENaC feature is sodium self-inhibition (SSI), a rapid autoregulatory mechanism in which extracellular Na ions allosterically bind ENaC and facilitate transition into a low open probability state. Although SSI is an important functional parameter for assessing ENaC activity and gating, its quantification has traditionally relied on manual two-electrode voltage-clamp (TEVC) recordings with limited scalability and throughput. Here, we improved and evaluated experimental strategies and analytical methods for robust quantification of ENaC SSI in manual and automated TEVC systems: (1) The determination of SSI from extrapolation of transient current recordings in response to a jump in the extracellular Na concentration; (2) the estimation of SSI by comparison of steady-state currents before and after chemical modification of a β-ENaC mutant with MTSET; and (3) quantification of SSI from the analysis of steady-state current-voltage relationships recorded at different extracellular Na concentrations. The latter procedure is the most reliable for SSI quantification in perfusion rate-limited automated TEVC systems. These methods can expand the capabilities of automated electrophysiology and support medium- to high-throughput investigation of autoregulatory mechanisms in ENaC variants and the discovery of novel ENaC modulators.
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3. High-salt diet modulates endocrine regulation between cortisol and FGF23.
3. 高盐饮食调节皮质醇与FGF23之间的内分泌调控PMID:日期:2026-09-19Excessive dietary salt intake is a global health concern, affecting cardiovascular, renal, and bone health. While the renin-angiotensin-aldosterone system (RAAS) is a known regulator of dietary salt-induced hormonal responses, the impact of adrenal cortisol remains unclear. Here, we performed a retrospective analysis in individuals (n = 321) consuming a random diet. Dietary salt intake positively correlated with urinary cortisol and inversely correlated with plasma fibroblast growth factor 23 (FGF23), a bone-derived hormone regulating phosphate and vitamin D homeostasis. Controlled salt diets in healthy individuals confirmed a dose-dependent increase in urinary cortisol and suppression of plasma FGF23. In mice, oral corticosterone, a cortisol analogue, reduced circulating FGF23 levels. RNA-seq analysis of corticosterone-treated MC3T3 osteoblasts identified suppression of FGF23 via glucocorticoid receptor activation, anti-inflammatory pathways, and reduced osteoblast activity. Our findings provide evidence for an endocrine cascade in which high salt intake elevates cortisol signaling and suppresses FGF23.
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4. A reporting checklist for human and animal heart rate variability research.
PMID:日期:2026-09-16Heart rate variability (HRV) is widely used as a non-invasive marker of cardiac autonomic regulation in human and experimental animal research. Its accessibility, repeatability, and applicability across clinical, psychophysiological, wearable, and preclinical settings make HRV a valuable translational tool. However, HRV indices are highly sensitive to physiological and methodological context, including recording duration, signal quality, respiratory pattern, posture, behavioral state, circadian timing, medication use, anesthesia, temperature, species, strain, artefact correction, frequency-band selection, and analytical method. Human HRV standards provide a strong methodological foundation, but they cannot be directly transferred to animal models without considering species-specific differences in basal heart rate, respiratory frequency, autonomic regulation, recording conditions, and experimental constraints. In animal studies, additional sources of heterogeneity include telemetry versus surface ECG recordings, conscious versus anesthetized states, handling and restraint, surgical recovery, body temperature control, and inconsistent frequency-domain definitions. This review synthesizes current methodological knowledge on HRV measurement in human and experimental animal studies and highlights major challenges that limit reproducibility and translational interpretation. Attention is given to common methodological pitfalls, and the risk of overinterpreting single indices such as LF/HF as direct measures of sympathovagal balance. We also propose a minimum reporting framework for human and experimental animal HRV studies, with shared translational items intended to support authors, reviewers, and editors. Transparent reporting of acquisition, preprocessing, analysis, and physiological context may improve comparability across studies and strengthen the role of HRV as a bridge between mechanistic animal research and human autonomic assessment.Clinical trial number: not applicable.
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5. The neurobiotic sense: emerging pathways of microbial detection and gut-brain communication.
PMID:日期:2026-09-12The gut microbiota, a complex community of bacteria, fungi, viruses, and other microorganisms, plays a critical role in regulating host physiology through the gut-brain axis. The gut microbiota interacts with the central nervous system through a range of interconnected pathways. These include humoral signaling, immune-related mechanisms, sensory afferent pathways, and the modulation of enteric neural circuits. Recent research has uncovered specialized epithelial sensory cells, like neuropod cells, that can directly detect microbial molecules and send signals via vagal afferents. This discovery highlights a previously unknown aspect of communication between the gut and brain. The review investigates the structural and functional diversity of the ENS, highlighting components like mechanosensory and chemosensory neurons, enteroendocrine cells, and neuropods that interact with vagal afferents. Specific focus is placed on pattern recognition receptors such as TLR5, which allow gut epithelial neuropod cells to sense bacterial flagellin and dynamically regulate appetite via PYY release and vagal signaling. Further examination addresses the impact of microbial metabolites including short-chain fatty acids, bile acids, tryptophan derivatives on neuronal excitability, neurotransmitter synthesis, and neuroimmune interactions. These insights underscore the gut as a sensory organ equipped with neural circuits specialized for detecting microbial cues, reimagining traditional concepts of host-microbe communication. By redefining microbial detection as a distinct sense comparable to vision or taste, the neurobiotic sense offers a transformative perspective on how gut microbes influence behavior, feeding patterns, and brain function. This emerging framework holds the potential to drive novel therapeutic strategies for treating metabolic, inflammatory, and neuropsychiatric disorders.
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6. ASIC currents in cultured primate retinal rod and cone cells.
PMID:日期:2026-09-05Acid Sensing Ion Channels (ASICs) are widely expressed in the nervous system and involved in an increasing number of functions such as nociception, mechanoreception, and taste transduction, to name a few. In the CNS, ASICs are involved in synaptic plasticity, learning/memory, and in acidosis-mediated neuronal injury. In retina, ASICs are expressed in rodent, rabbit and monkey retina and pharmacological and gene knockdown studies have indicated changes in the earliest phases of electroretinogram that point to effects on phototransduction. This finding led us to investigate the electrophysiological/pharmacological properties of ASICs in cultured primate rod and cone cells. Patch-clamp recordings showed transient ASIC currents with a threshold pH of ~ 7.0 and pH of 6.15 ± 0.03 and 6.33 ± 0.03 for cultured rod and cone cells, respectively. The currents were almost completely blocked by amiloride and highly sensitive to PcTx-1. Our results for the first time demonstrate the expression of functional ASICs on primate photoreceptors and suggest that ASIC currents in these cells are mediated predominantly by homomeric ASIC1a channels.
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7. Palmitoylethanolamide supplementation partly modulates eccentric exercise-induced changes in the bioactive lipid profile of skeletal muscle tissue.
PMID:日期:2026-08-28Strenuous exercise induces microstructural muscle damage, leading to delayed onset muscle soreness and reduced performance. Although structural changes are well documented, subsequent inflammatory responses are not fully understood. Research has mainly examined leukocyte infiltration and cytokine expression, while low-abundance bioactive lipid mediators remain understudied. Nutritional strategies, such as palmitoylethanolamide (PEA) supplementation, can modulate these mediators and promote anti-inflammatory, pro-resolving conditions, which may improve recovery. Therefore, the present study evaluated the effect of PEA on the abundance of bioactive lipid mediators in skeletal muscle tissue of healthy males following muscle damaging exercise (MDE). 10 participants were included in a double-blind crossover study where they received PEA (2 × 350 mg/d, Levagen+) or placebo (PLA, maltodextrin), in a randomized order. In each experimental condition participants performed an MDE bout (24 × 10 eccentric contractions of the knee extensors on an isokinetic dynamometer). Muscle biopsies were collected at baseline and 48 h following MDE and analysed for lipid mediator profile via LC-MS/MS-based lipidomics. Many lipid mediators decreased 48 h post-exercise in PLA, whereas they remained unchanged or increased in PEA. This pattern was observed for mediators derived from AA (12-HHTrE, 11-HETE, 12-HETE, 15-HETE, 15-epi-LXA4, 14,15-EpETrE, 5,6-DiHETrE), DHA (4-HDoHE), LA (9-HODE, 13-HODE) and ALA (9-HOTrE, 13-HOTrE). MCTR3 levels were consistently higher in PEA compared to PLA, whereas concentrations of LXB4 and AT-RvD3 were consistently lower in PEA compared to PLA, independent of exercise. In conclusion, PEA supplementation attenuated or counteracted the decline in lipid mediators following exercise, indicating that PEA partially enhances bioactive lipid tone in response to strenuous exercise.
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8. Acid Sensing Ion Channels (ASICs) in the brain: emerging roles in physiology and pathology.
PMID:日期:2026-08-26While under physiological conditions, extracellular pH in the brain is reasonably constant, several mechanisms induce transient and localized pH fluctuations. Multiple pathologies involve prolonged changes in pH. Therefore, detecting and monitoring pH changes is crucial for the proper functioning of the nervous system. Acid-Sensing Ion Channels (ASICs) are Na+-permeable ion channels, predominantly expressed in the nervous tissue and activated by protons. Thus, ASICs act as pH sensors, leading to neuronal excitation when the pH drops. ASICs belong to the epithelial sodium channel/degenerin (ENaC/DEG) family of amiloride-sensitive transmembrane ion channel proteins. There are at least eight different ASIC subunits encoded by five genes. Functional ASICs assembled in the plasma membrane are homo- or heteromeric trimers. Trimers containing ASIC1a are of particular interest as, in addition to sodium ions, they also conduct calcium ions and thus can regulate multiple cellular processes. ASICs are involved in numerous physiological functions and pathological states. Biophysical properties of ASICs, their evolutionary origins, regulation and pharmacology, their roles in the peripheral nervous system and in the regulation of synaptic transmission have been recently reviewed in many details. Here we shall focus on brain ASICs in the context of the following issues. (i) The role of ASICs in the homeostasis of extracellular рН in the brain; (ii) interactions of ASICs with major neurotransmitters and (iii) ASICs as emerging key factors and drug targets in brain pathology with focus on stroke, neurological consequences of neonatal hyperbilirubinemia, and Alzheimer's disease.
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9. Pendrin inhibitor PDSinh-C01 reverses salt-sensitive hypertension and metabolic acidosis in the 5/6 nephrectomy rat model.
PMID:日期:2026-08-17Pharmacological inhibition of the chloride-bicarbonate exchanger pendrin with PDSinh-C01 potentiates the diuretic action of furosemide in healthy mice. Because pendrin contributes to acid-base regulation and blood pressure control, it may represent an attractive therapeutic target in chronic kidney disease (CKD). We investigated whether this pendrin inhibitor improves metabolic acidosis and salt-sensitive hypertension in the 5/6 nephrectomy (5/6Nx) model of CKD. Seven-week-old female Sprague Dawley rats underwent 5/6Nx and implantation of telemetry devices for blood pressure monitoring. All animals received a high-salt (2% NaCl) diet and were randomized (n = 7-9/group) to daily subcutaneous injections for three days of vehicle, PDSinh-C01 (10 mg/kg), furosemide (6 mg/kg), or their combination. The 5/6Nx model recapitulated key features of CKD, including reduced eGFR, hypertension, proteinuria, and hyperchloremic metabolic acidosis. Combination therapy produced the greatest reduction in mean arterial pressure (-11 ± 2 mmHg) compared with vehicle (-3 ± 2 mmHg), furosemide (-6 ± 1 mmHg), or pendrin inhibitor alone (-6 ± 2 mmHg). Furosemide and combination therapy increased urine volume at 6h, whereas only combination therapy increased urine volume at 24h. After three days, the pendrin inhibitor alone and combination therapy increased venous bicarbonate concentrations compared with vehicle (24.5 ± 2.1 and 24.3 ± 1.4 vs. 21.4 ± 1.4 mmol/l). In conclusion, PDSinh-C01 combined with furosemide improves salt-sensitive hypertension in CKD, while PDSinh-C01 alone and in combination with furosemide ameliorates metabolic acidosis. These findings support pendrin as a regulator of electrolyte and acid-base balance and as a potential therapeutic target in CKD.
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10. NAPE-PLD: the healthy intersection of N-acylethanolamines and bile acids in physiology and diseases.
PMID:日期:2026-08-15Linking the distinctive structural and functional properties of lipids belonging to different signaling classes is a frontier of physiology. The present minireview focuses on the endocannabinoidome phospholipase NAPE-PLD, which has bile acids (BAs) as structural cofactors at membrane interface and generates bioactive N-acylethanolamines (NAEs) that promote pleiotropic effects. NAPE-PLD is thus at the crossroads of both their physiological functions, an area of ongoing research. The wide internal channel of NAPE-PLD facilitates the transmembrane transport of pyridoxal 5'-phosphate (PLP) and can support the activity of PLP-dependent enzymes in mitochondria, peroxisome and other subcellular compartments. Recent insights demonstrate that drugs and agents that stabilize NAPE-PLD can control blood pressure, vascular resistance and cardiovascular morbidity in clinics, offering new perspectives on the interaction between NAEs and BAs in cardiometabolic and neurological disorders.