Pflugers Archiv : European journal of physiology最新文献

{"title":"Biphasic regulation of myogenesis by ALDH2, aldosterone, and oxidative stress.","authors":"José Emmanuel Martínez-Cortés, Maikel Valle-Clara, Damaso Fernández-Hernández, Guillermo Ávila","doi":"10.1007/s00424-026-03185-w","DOIUrl":"10.1007/s00424-026-03185-w","url":null,"abstract":"<p><p>Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme that metabolizes 4-hydroxynonenal (4-HNE), a lipoperoxidation-derived aldehyde that promotes oxidative stress. ALDH2 is therefore considered part of the antioxidant defense. On the other hand, the hormone aldosterone enhances the production of reactive oxygen species (ROS) in many cell types. During skeletal muscle development (myogenesis), myoblasts fuse to form multinucleated cells, called myotubes. In the present study, we investigated the potential of ALDH2 to regulate ROS production in C2C12 cells and its effects on myotube formation during early (0-3 days) and late (4-9 days) stages. Western blot results indicate that these cells actually express ALDH2. Interestingly, incubating cells (1.5-24h) with the pro-oxidant compounds H₂O₂, 4-HNE, aldosterone, and daidzin (ALDH2 antagonist) enhanced ROS production. In contrast, two ALDH2 agonists (Alda-1 and AD-5591) prevented, with similar potency, the 4-HNE- and aldosterone-induced oxidative stress. We next demonstrated that incubating cells with H₂O₂ (0.5-5 µM) induces a biphasic regulation of myotube formation, with early inhibition and late stimulation. This H₂O₂-induced biphasic regulation was also reproduced by aldosterone, daidzin, and another ALDH2 antagonist (CVT-10216). Consistent with their effects on oxidative stress, the ALDH2 agonists Alda-1 and AD-5591 eliminated the regulation of myoblast fusion by H₂O₂ and aldosterone. Additional data suggest that aldosterone acts through the mineralocorticoid receptor, and both calpain and p38-MAPK are also implicated. These findings indicate that ALDH2 is essential for regulating oxidative stress in myogenic cells and is involved in a signaling pathway that governs myoblast fusion through biphasic and opposing mechanisms.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148205809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"First-in-human to proof-of-concept: why experimental medicine studies remain essential in human physiology and drug development.","authors":"Robert J Unwin, Benjamin Challis, Carsten Wagner, Giovambattista Capasso, Stefan Carlsson","doi":"10.1007/s00424-026-03184-x","DOIUrl":"10.1007/s00424-026-03184-x","url":null,"abstract":"<p><p>Experimental medicine studies, small, mechanistically focused investigations, have historically driven key discoveries in human physiology and pharmacology. Despite their foundational role, these studies are increasingly marginalised in today's drug development environment due to economic pressures, regulatory conservatism, and an overemphasis on statistical endpoints from large-scale trials. This article traces the historical roots and enduring value of experimental medicine, distinguishes it from current early phase drug development studies, and explores the structural forces behind its decline. N-of-1 trials are discussed as a systematic extension of these principles, offering precision insights at the individual level. We apply this discussion to chronic kidney disease (CKD), a field where slow progression and heterogeneous pathophysiology make early mechanistic studies especially valuable. We argue that bypassing such studies in favour of speed represents a strategic gamble that may misdirect costly late-phase trials. Integrating mechanistic insights with statistical power is not superfluous, but essential, particularly in complex diseases like CKD where understanding why and how interventions work may matter as much as whether they do. We acknowledge that achieving this vision necessitates overcoming significant structural, economic, and cultural barriers within the current drug development environment; however, the costs of inaction, manifest as trial failures, patient harm, and missed therapeutic opportunities, are potentially much greater.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13236740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148157218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parathyroid hormone enhances appetite and fails to reduce adiposity in ob/ob mice.","authors":"Abul Fajol, Hirotaka Komaba, Chigusa Ishioka, Yosuke Nakagawa, Naoto Hamano, Takehiko Wada, Masafumi Fukagawa","doi":"10.1007/s00424-026-03183-y","DOIUrl":"10.1007/s00424-026-03183-y","url":null,"abstract":"<p><p>Obesity is a major driver of type 2 diabetes, underscoring the urgent need for therapies that target both energy expenditure and glucose homeostasis. Parathyroid hormone (PTH) has been implicated in promoting adipose tissue browning and thermogenesis, but its metabolic impact in the context of obesity remains uncertain. We aimed to examine the effects of PTH in ob/ob mice, a leptin-deficient model of obesity and diabetes. A single dose or daily injections of human PTH(1-34) were administered to ob/ob mice and their wild-type littermates. Metabolic outcomes, adipose tissue thermogenesis, and appetite-regulating pathways were assessed. A pair-feeding study was also performed to isolate the effect of PTH from food intake. A single acute dose of PTH upregulated thermogenic gene expression in adipose tissue in a dose-dependent manner. However, repeated daily PTH administration failed to sustain adipose browning or improve insulin resistance and hyperglycemia; instead, it exacerbated weight gain, primarily due to increased food intake. Mechanistically, PTH enhanced gastric ghrelin production and upregulated hypothalamic AgRP expression, suggesting a central orexigenic effect. In pair-feeding experiments, PTH-treated mice showed no significant improvements in adiposity or metabolic parameters, even when caloric intake was matched. Although PTH transiently promotes thermogenesis in adipose tissue in ob/ob mice, sustained exposure exacerbates hyperphagia without meaningful metabolic benefit. These findings highlight the challenges of targeting PTH signaling for treating obesity-related diabetes.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13230290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oestrogen receptors regulate vascular β₁- and β₃-adrenoceptor expression and shape sex-specific adrenergic control of vascular tone.","authors":"Kristin Riedel, Andreas Deussen, Birgit Zatschler, Carmen Hentsche, Bianca Müller, Stephan Speier, Christian Reeps, Sems M Tugtekin, Klaus Matschke, Irakli Kopaliani","doi":"10.1007/s00424-026-03182-z","DOIUrl":"10.1007/s00424-026-03182-z","url":null,"abstract":"<p><p>Sex differences in vascular adrenergic responsiveness contribute to differential regulation of vascular tone. Female vessels exhibit enhanced β-adrenergic relaxation compared with males, but the role of oestrogen receptors in maintaining this phenotype and the capacity of sex hormone exposure to reprogram vascular β-adrenoceptor expression remain incompletely understood. Thoracic aorta and mesenteric arteries from Wistar Kyoto rats were examined following pharmacological oestrogen receptor inhibition or cross-sex hormone treatment. Vascular reactivity was assessed using wire myography, and β₁-, β₂-, and β₃-adrenoceptor mRNA expression was quantified by qPCR. Oestrogen receptor blockade with fulvestrant enhanced norepinephrine-induced vasoconstriction and reduced β-adrenergic relaxation in both conduit and resistance arteries. These functional alterations were accompanied by an approximately 50% reduction in β₁- and β₃-adrenoceptor mRNA expression, whereas β₂ expression remained unchanged. Conversely, oestrogen treatment in males attenuated vasoconstriction, enhanced β-adrenergic relaxation, and increased β₁- and β₃-adrenoceptor expression, while testosterone treatment in females had no effects. Despite pronounced vascular changes, arterial blood pressure remained unaltered. Analysis of human aorta, carotid, iliac, and mammary arteries revealed consistently higher β₁- and β₃-adrenoceptor mRNA expression in women compared with men. Oestrogen receptor inhibition reduces vascular β₁- and β₃-adrenoceptor expression and impairs β-adrenergic vasodilation, thereby shifting adrenergic vascular responses towards enhanced constriction. Conversely, oestrogen exposure reprogrammes the male vascular phenotype towards a female-like β-adrenergic profile. These findings identify an oestrogen receptor-dependent β₁/β₃-adrenoceptor axis as a conserved mechanism underlying sex-specific regulation of vascular tone.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13194341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147988629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KCa3.1 mediates radioresistance of silver nanoparticles in human glioblastoma cells.","authors":"Francesco Ragonese, Andrea Biagini, Luana Sallicandro, Alessandra Mirarchi, Gianmarco Reali, Antonella De Luca, Cataldo Arcuri, Sara Flamini, Oxana Bereshchenko, Paolo Cogliati, Roberto Spogli, Paola Sabbatini, Stefano Bruscoli, Paolo Sportoletti, Bernard Fioretti","doi":"10.1007/s00424-026-03179-8","DOIUrl":"10.1007/s00424-026-03179-8","url":null,"abstract":"<p><p>Silver nanoparticles (AgNPs) have emerged as a promising therapeutic tool for managing glioblastoma (GB), particularly in radiosensitisation. However, their mechanisms of action are not yet fully understood. Since ion channel activity is implicated in various aspects of radioresistance, we investigated the electrophysiological effects of AgNPs on GB cells. In the U251 human GB cell line, the acute application of AgNPs induced the activation of a cationic nonselective current in a dose-dependent manner, which was not affected by ACA (TRPM2 blocker). In addition, AgNPs increased intracellular calcium concentration, caused depolarisation of the mitochondrial inner membrane, and promoted membrane blebbing. The investigation revealed that calcium influx is a critical step in the AgNPs-induced effects. Thiol reagents such as cysteine are known silver chelating agents and their application prevented the activation of cationic currents, intracellular calcium increases, and membrane blebbing formation induced by AgNPs. This finding suggested Ag⁺ are the active species responsible for these effects, acting through IAg current previously characterized in our laboratory. Intracellular calcium influx induced by AgNPs activated intermediate-conductance calcium-activated potassium currents. This activation was accordingly blocked by TRAM-34, a selective inhibitor of KCa3.1 channels. Finally, AgNPs were found to reduce U251-GB cell viability in a dose-dependent manner and to increase G2/M phase accumulation following sublethal irradiation. In the presence of TRAM-34 the G2/M phase accumulation induced by the combined treatment with AgNPs and irradiation was reduced, suggesting the involvement of radioresistance-associated KCa3.1 currents. These results provide new insights into optimizing the use of AgNPs as radiosensitizing agents in GB therapy.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic atorvastatin treatment weakens procontractile influence of NADPH oxidase derived ROS in systemic murine arteries.","authors":"Anastasia A Shvetsova, Guzalia F Zakirjanova, Kseniia P Ostapchuk, Alexey M Petrov, Dina K Gaynullina","doi":"10.1007/s00424-026-03181-0","DOIUrl":"10.1007/s00424-026-03181-0","url":null,"abstract":"<p><p>The beneficial effects of statins for cardiovascular system were widely described in various pathologies. However, much less is known about the effects of statins in healthy organism, especially in systemic resistance arteries. We aimed to evaluate the effect of chronic administration of atorvastatin, one of the most prescribed drugs, on the arterial functioning in various organs (brain, small intestine, skeletal muscle) of mice, including the procontractile influence of NADPH oxidase derived reactive oxygen species (ROS) as well as Rho-kinase. Mature male outbred ICR(CD-1) mice were administered with atorvastatin during 4 weeks (daily dose ⁓ 7 mg/kg), control animals drank water with its solvent DMSO (0.3% v/v). Basilar, sural and mesenteric arteries were studied by wire myography and/or qPCR. Atorvastatin treatment led to the reduction of contractile responses to thromboxane A2 receptor agonist U46619 in basilar arteries, but did not change responses of sural and mesenteric arteries to α1-adrenoceptor agonist methoxamine. Endothelium-dependent relaxation to acetylcholine was not altered in all studied arteries. Procontractile contribution of NADPH oxidase derived ROS was weakened in all arteries in atorvastatin group of animals, that was associated with the reduced procontractile influence of Rho-kinase in basilar arteries, but not sural and mesenteric. mRNA values of catalytic Nox2 and Nox4 subunits in mesenteric arteries were not changed due to atorvastatin treatment. Therefore, chronic atorvastatin treatment during one month affects the mechanisms regulating vascular tone in healthy mice, which must be taken into account when prescribing statin therapy to healthy people for preventive purposes.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spexin disrupts migrating myoelectric complex in the rat small intestine: The role of galanin-2 and muscarinic receptors.","authors":"Özge Darakcı Saltık, Hakan Balcı, Rümeysa Abdullahoğlu, Ayhan Bozkurt","doi":"10.1007/s00424-026-03180-1","DOIUrl":"10.1007/s00424-026-03180-1","url":null,"abstract":"<p><p>Spexin (SPX) is an endogenous peptide expressed throughout the gastrointestinal tract. Although its impact on postprandial intestinal motility has been examined, its effect during fasting remains unclear. This study aimed to investigate the direct effects of SPX on jejunal and ileal segments in vitro, its effects on fasting small intestinal motility in vivo, and to determine the roles of galanin-2, muscarinic, and 5-hydroxytryptamine-3 (5-HT₃) receptors in these actions. The contractile responses of rat jejunal and ileal segments to SPX (10⁻⁹-10⁻⁶ M), with or without pretreatment with galanin-2, muscarinic, or 5-HT₃ receptor antagonists (M871, atropine, and ondansetron, respectively) were evaluated in organ baths. For in vivo experiments, bipolar electrodes were implanted at two jejunal sites to record migrating myoelectric complexes (MMC), and a catheter was inserted into the left jugular vein for drug administration. SPX (40-640 µg/kg/h) was infused for 1 hour following basal MMC recording. Antagonists were administered 5 minutes prior to SPX (320 µg/kg/h) infusion. SPX induced concentration-dependent contractions in both intestinal segments, significantly inhibited by M871 but unaffected by atropine or ondansetron. At 160 μg/kg/h, SPX altered the MMC pattern; at 320 μg/kg/h, it disrupted MMC and induced irregular spiking activity, which was blocked by M871 and atropine, but not by ondansetron. These data indicate that SPX modulates fasted motility pattern, involving GALR2-dependent mechanisms and an indirect contribution of muscarinic pathways. These findings may support the development of therapies for gastrointestinal motility disorders.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 6","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13183699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise-induced microRNAs: molecular pathways and adaptive remodeling of skeletal muscle.","authors":"Kübra Özdemir, Yeliz Demir","doi":"10.1007/s00424-026-03177-w","DOIUrl":"10.1007/s00424-026-03177-w","url":null,"abstract":"<p><p>Exercise is an effective physiological stimulus that promotes vast structural and functional changes in skeletal muscular tissue. Although transcriptional pathways that control exercise-based plasticity have been studied in depth, recent findings highlight the importance of microRNAs (miRNAs) as an essential post-transcriptional control platform mediating contractile stimuli and molecular and physiologic adaptations. This review provides a synthesis of existing evidence on exercise responsive miRNAs at the systems level, and especially on the topic of skeletal muscle remodeling. The review outlines the effects of different exercise regimens such as endurance, resistance, and high-intensity interval training to dynamic miRNA response to regulate major biological pathways such as mitochondrial biogenesis, protein turnover, angiogenesis, inflammatory signaling, and metabolic regulation. Acute exercise is also typified by temporary changes in miRNAs, which facilitate short-term stress signalling, and chronic training leads to more long-term miRNA re-programming, which facilitates long-term structural and functional remodeling. Also, circulating and exosome-bound miRNAs are also mentioned as potential agents of the muscle-to-organ interaction, thus supporting the idea of skeletal muscle that acts like an endocrine-like organ during exercise. Besides narrative synthesis, the review is based on an exploratory, data-driven re-analysis of publicly available skeletal muscle miRNA sequencing data to define convergent regulatory programs instead of data-specific differentiation. This is observed under integrative pathway and network-level analysis which identifies coordinated miRNA modules linked to mitochondrial regulation, cytoskeletal remodeling, and inflammatory control. Taken together, this framework brings together non-homogenous evidence throughout the literature and highlights the prospect of exercise-sensitive miRNAs as systems-level regulators of skeletal muscle adaptation.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of IP₃R and TRPC3 channels in vasoconstriction and hypertension.","authors":"Raiana Dos Anjos Moraes, Quiara Lovatti Alves, Liliane Barreto da Silva, Rafael Leonne Cruz de Jesus, Darízy Flávia Silva","doi":"10.1007/s00424-026-03175-y","DOIUrl":"10.1007/s00424-026-03175-y","url":null,"abstract":"<p><p>Hypertension is a major global health concern and a leading risk factor for cardiovascular diseases, including stroke, myocardial infarction, and heart failure. A hallmark of hypertension is elevated total peripheral vascular resistance, often driven by sustained and abnormal vasoconstriction. Calcium ions (Ca²⁺) play a central role in vascular smooth muscle cell (VSMC) contraction, and their intracellular concentration is tightly regulated by multiple signaling pathways. Among these, the inositol 1,4,5-trisphosphate receptor (IP₃R) and the transient receptor potential canonical type 3 (TRPC3) channel are critical mediators of Ca²⁺ signaling. IP₃R activation triggers Ca²⁺ release from the endoplasmic reticulum, while TRPC3 channels facilitate Ca²⁺ and Na⁺ influx across the plasma membrane. Several studies have shown that both IP₃Rs and TRPC3 channels are upregulated in hypertensive animal models. Human studies have also demonstrated elevated TRPC3 expression in the context of pulmonary arterial hypertension (PAH). This review provides a comprehensive overview of the structural domains and membrane microdomains that facilitate IP₃R-TRPC3 coupling and Ca²⁺ influx. IP₃ and endothelin-1 stimulate TRPC3 channels and promote their molecular coupling to IP₃Rs, leading to activation of nonselective cation currents in artery myocytes. Increased expression and/or activity of IP₃Rs and TRPC3 channels amplifies this signaling, contributing to the increased vascular tone characteristic of the hypertensive state. Understanding the molecular interplay between IP₃Rs and TRPC3 channels offers new insight into the dysregulated Ca²⁺ signaling underlying hypertension. Targeting this coupling mechanism may represent a novel therapeutic strategy to restore vascular homeostasis and reduce blood pressure in affected individuals.</p>","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147819509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin converting enzyme-2 activation mitigates glucocorticoids-induced osteoporosis in rats by modulating oxidative stress, inflammation and the RANKL/OPG pathway.","authors":"Heba Fathy El-Domiaty, Mohamed Abdallah, Nesrin Abd Allah Salman, Walaa Abdellah Esa, Doaa Abdelsatar Madkour, Eman I Elgizawy","doi":"10.1007/s00424-026-03167-y","DOIUrl":"10.1007/s00424-026-03167-y","url":null,"abstract":"","PeriodicalId":19954,"journal":{"name":"Pflugers Archiv : European journal of physiology","volume":"478 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147778222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}