Acta Physiologica最新文献

{"title":"Hexosamine Pathway as a Therapeutic Strategy in Primary Mitochondrial Encephalopathy","authors":"Henver S. Brunetta","doi":"10.1111/apha.70196","DOIUrl":"10.1111/apha.70196","url":null,"abstract":"<p>The central nervous system (CNS) has an extraordinarily high energetic demand and consumes around 20% of whole-body resting oxygen consumption, while accounting for merely ~2% of body mass. As a result, it is not surprising that CNS cells (neurons, astrocytes, microglia, etc.) are well equipped with great mitochondrial content to support many of the energy-consuming cellular processes, including synapses, axonal branching and transport, membrane potential polarization, ion transport, and others [<span>1</span>]. Unfortunately, the great reliance on mitochondrial bioenergetics comes with a wide number of primary mitochondrial neurological syndromes, such as mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes (MELAS), myoclonic epilepsy with ragged-red fibers (MERRF), Leigh syndrome, Chronic progressive external ophthalmoplegia (CPEO), and others [<span>2</span>]. In addition to primary mitochondrial neurological syndromes, common late-onset brain diseases, including Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis, can also involve mitochondrial mutations [<span>3</span>]. The evidence ranges from pure bioenergetics defects to mitochondrial quality control, retrograde signaling, calcium buffering capacity, and redox homeostasis.</p><p>In this issue of <i>Acta Physiologica</i>, Jiménez-Sánchez et al. [<span>4</span>]. investigated the development of a primary mitochondrial fatal encephalopathy using a mouse model with a mutation in Coq9, the enzyme responsible for the biosynthesis of the coenzyme Q (Q10) (Figure 1a). The study addresses a series of provocative questions with broad-spectrum implications. For instance, what is the temporal relationship between cellular changes and symptoms? What are the main structural and cellular organizations affected by mitochondrial dysfunction? Is there a hierarchical set of components more susceptible to failure in such conditions? Answering these questions is fundamental to establishing causality as well as to improving treatment for patients suffering from primary mitochondrial neurological syndromes.</p><p>The authors provide a detailed timeline of pathological events, demonstrating that neuronal loss in the cortex, myelin damage, and astrocyte activation in the brainstem occur early (ca. 1 month of age) in this model, and precede the onset of motor symptoms. Interestingly, microglial activation appeared in late stages of neurological impairment, clarifying the cellular cascade initiated by this specific genetic defect (Figure 1a). Based on these findings, it could be informative to dissect cell-type composition during the progression of the neurodegeneration. For example, by co-staining NF-kB p65 with GFAP and Iba1 in the cortex and brainstem to quantify nuclear localization per cell type. This approach would provide per-cell pathway activation and partially control for compositional effects in aggregate measurements.</p><p>The mitochon","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147471900","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":"Home-Based Inspiratory Muscle Training Can Restore Cardiac Autonomic Balance and Improve Spontaneous Breathing Pattern in Post-COVID Individuals","authors":"Thais Dillinger Conway Santanna, André Luiz Musmanno Branco Oliveira, Pedro Paulo da Soares, Gabriel Dias Rodrigues","doi":"10.1111/apha.70199","DOIUrl":"10.1111/apha.70199","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462502","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":"Sex Differences in the Effects of Etonogestrel on Respiratory Recovery in an In Vivo Rat Model of Central Chemoreflex Impairment","authors":"Silvia Cardani,&nbsp;Tara A. Janes,&nbsp;Ryaad Asif,&nbsp;Silvia Pagliardini","doi":"10.1111/apha.70194","DOIUrl":"10.1111/apha.70194","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Rhythmic breathing movements driven by the brainstem rely on chemosensory inputs to homeostatically adjust motor output to the prevailing metabolic demand. The central CO₂ chemoreflex is a critical component of this neural circuitry, as defects in these sensors cause hypoventilation syndromes, which are typically difficult to manage pharmacologically. Progesterone has long been known to stimulate breathing in both sexes, and remarkably the progestinic metabolite, etonogestrel (ETO), enhances CO₂ chemosensitivity in animal models and female patients affected by congenital central hypoventilation syndrome. However, ETO‘s mechanisms and sites of action remain unknown, and the experimental use of synthetic progestins has been met with mixed respiratory outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In our recent work, we demonstrated that chronic ETO treatment improved the CO₂ chemoreflex in female rats in which &lt; 80% of chemoreceptor neurons comprising the retrotrapezoid nucleus (RTN) were eliminated. Since the progesterone receptor is widely expressed in both the male and female brain, we investigated whether ETO-induced CO₂ chemoreflex recovery can be replicated in male rats in which RTN neurons are partially eliminated by the use of substance P-saporin toxin.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our results confirm dose-dependent impairment of the CO₂ chemoreflex in both sexes following chemoreceptor lesion and corroborate the findings that ETO treatment restores ventilation in female rats with moderate-sized lesions. Interestingly, female respiratory recovery was associated with increased expression of the pH-sensing genes <i>Gpr4</i> and <i>Task2</i> in the RTN.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In contrast, male rats failed to show significant recovery with ETO treatment, suggesting a sex-specific mechanism through which ETO promotes CO₂ chemoreflex recovery.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12984012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147441988","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":"Pravastatin Corrects Endothelial Dysfunction in Ex Vivo Uterine Radial Arteries in Preeclampsia","authors":"Nathan M. Luque,&nbsp;Leo Leader,&nbsp;Sandra M. Lowe,&nbsp;Steven D. Horrowitz,&nbsp;Marianne Tare,&nbsp;Victoria Hinkley,&nbsp;Vladimir V. Matchkov,&nbsp;Maged M. Costantine,&nbsp;Irit Markus,&nbsp;Lu Liu,&nbsp;Shaun L. Sandow,&nbsp;Timothy V. Murphy","doi":"10.1111/apha.70186","DOIUrl":"10.1111/apha.70186","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Endothelium-dependent relaxation in isolated uterine radial arteries from normotensive (NT) and preeclamptic (PE) pregnancies, and the acute effects of pravastatin in the latter vessels were assessed. Pravastatin is hypothesized to alleviate endothelial dysfunction in PE via modulating aspects of NO and endothelium-derived hyperpolarization-mediated relaxation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Radial arteries isolated from the uterus of NT and PE pregnant patients were incubated with pravastatin (2 mM/6 h), methyl-β-cyclodextrin (10 mM/1 h) in vitro, or vehicle. Vessel function was determined with pressure myography, while related morphology and protein/mRNA expression were characterized using immunohistochemistry, electron microscopy, and qPCR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Endothelium-dependent, bradykinin-induced NO-mediated relaxation was impaired in radial arteries from PE compared to NT pregnancy, with a reduced intermediate- and large-conductance Ca²⁺-activated K⁺-channel contribution. Endothelial small-conductance Ca²⁺-activated K⁺-channel function and expression were increased in arteries from PE, compared to NT patients. Pravastatin restored NO and endothelium-derived hyperpolarization-mediated relaxation in arteries from PE women; potentially overcompensating overall endothelium-dependent relaxation. Myoendothelial gap junction and endothelial caveolae density, and caveolin-1 and endothelial-NOS expression were decreased in arteries from PE relative to NT pregnancies and increased following pravastatin incubation. Caveolae density in NT patient arteries was reduced by methyl-β-cyclodextrin, while endothelial caveolae were increased in vessels from PE patients. Pravastatin incubation restored endothelial function via improved NO and endothelium-derived hyperpolarization-type mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Pravastatin restored endothelium-dependent relaxation in uterine radial arteries from PE pregnancies. Data support the therapeutic potential for pravastatin in treating PE, with ongoing trials determining the validity of its use in the clinical setting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>ClinicalTrials.gov identifier: NCT01717586</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12976587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147429463","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":"Correction to “N-Acetylglucosamine Selectively Attenuates Neuroinflammation in a Mouse Model of Mitochondrial Dysfunction”","authors":"","doi":"10.1111/apha.70201","DOIUrl":"10.1111/apha.70201","url":null,"abstract":"<p>L. Jiménez-Sánchez, P. Ruiz-López, P. González-García, et al., “N-Acetylglucosamine Selectively Attenuates Neuroinflammation in a Mouse Model of Mitochondrial Dysfunction,” Acta Physiologica 242, no. 3 (2026): e70179, https://doi.org/10.1111/apha.70179.</p><p>In the published version, affiliations 1 and 2 appear in the incorrect order. The correct order should be:</p><p>1. Department of Physiology, Facultad de Medicina, Universidad de Granada, Granada, Spain</p><p>2. Instituto de Investigación Biosanitaria ibs.Granada, Granada, Spain</p><p>The correct affiliation numbers in the author byline are:</p><p>Paula Ruiz-López^1,3</p><p>Juan Manuel Martínez-Galvez^1,3,5</p><p>Enrica Olivieri^1,3</p><p>The complete corrected author list and affiliations are as follows:</p><p>Laura Jiménez-Sánchez^1,2,3| Paula Ruiz-López^1,3| Pilar González-García^1,2,3| JannePurhonen⁴| Juan Manuel Martínez-Gálvez^1,3,5| Sergio López-Herrador^1,2,3| Julia Corral-Sarasa^1,2,3| María Elena Díaz-Casado^1,2,3| Carmen Venegas^1,2,3| Isaac Santos-Pérez⁶| Enrica Olivieri^1,3| Adriana L. Rojas⁶| Luis Carlos López^1,2,3,7</p><p>¹Departament of Physiology, Facultad de Medicina, Universidad de Granada, Granada, Spain |²Instituto de Investigación Biosanitaria ibs.Granada, Granada, Spain |³Instituto de Biotecnología, Centro de Investigación Biomédica, Universidad de Granada, Granada, Spain|⁴Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden|⁵Biofisika Institute (CSIC, UBV-EHU) and Department of Biochemistry and Molecular Biology, University of Basque Country, Leioa, Spain|⁶Electron Microscopy and Crystallography, Center for Cooperative Research in Biosciences (CIC bioGUNE), Bizkaia Science and Technology Park, Derio, Bizkaia, Spain|⁷Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable (CIBERFES), Granada, Spain</p><p>We apologize for this error.</p>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147429500","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":"Tacrolimus Induced Hypertension and Vascular Remodeling Includes Mechanisms of Cellular Senescence—The Protective Effect of Valsartan","authors":"Lingyan Fei,&nbsp;Xiaohua Wang,&nbsp;Lingyi Kong,&nbsp;Tianjiao Cui,&nbsp;Pratik H. Khedkar,&nbsp;Yunxiu Xiang,&nbsp;Dongliang Zhao,&nbsp;Junxuan Fang,&nbsp;Yulin Liang,&nbsp;Yangyang Zhang,&nbsp;Nan Xu,&nbsp;Xingyu Qiu,&nbsp;Liang Zhao,&nbsp;Gensheng Zhang,&nbsp;Yan Lei,&nbsp;Chun Tang,&nbsp;Kongyang Ma,&nbsp;Liwei Lu,&nbsp;Jin Wei,&nbsp;En Yin Lai,&nbsp;Pontus B. Persson,&nbsp;Andreas Patzak,&nbsp;Zhihua Zheng,&nbsp;Shan Jiang","doi":"10.1111/apha.70189","DOIUrl":"10.1111/apha.70189","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Calcineurin inhibitors (CNI) such as tacrolimus (Tac) are the first-line treatment to prevent transplant rejection. However, CNI have adverse effects on blood vessels and renal function, which may be linked to cellular senescence. Valsartan, a common angiotensin II type 1 receptor (AT₁R) blocker, exhibits anti-senescence properties. We tested the hypothesis that tacrolimus causes hypertension and microvascular remodeling that involves induction of senescence, and that valsartan is protective.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Microperfusion and wire myography were employed to assess the contractile and dilatory functions of renal afferent arterioles (Af-Art) and mesenteric arteries, respectively. The expression of components of the renin-angiotensin system (RAS) and senescence-associated biomarkers was investigated using qPCR and immunohistochemistry.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Long-term administration of Tac activated the RAS. Tac-induced microvascular remodeling in mesenteric arteries and Af-Art was mitigated by treatment with valsartan. Mice treated with Tac exhibited increased vasoconstriction in response to angiotensin II and reduced dilation to acetylcholine. Both effects were abolished by valsartan. Additionally, senescence-associated biomarkers were upregulated in mesenteric and renal resistance arteries from Tac-treated mice. Co-administration of Tac with valsartan or ABT-263, a senolytic agent, rescued Tac-induced microvascular injury and reduced hypertension (conscious mice, noninvasive tail-cuff system). Treatment with the antihypertensive drug amlodipine normalized blood pressure and downregulated senescence-associated beta-galactosidase in mesenteric arteries.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that cellular senescence contributes to Tac-induced microvascular injury and hypertension and demonstrate the effectiveness of senolytic treatment for protection. Valsartan could reduce senescence indirectly by lowering blood pressure; a direct anti-senescence effect might also play a role in this context.</p>\u0000 </section>\u0000 </div>","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147429442","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":"Cell Type Dependent Regulation of Neuronal Activity via SIRT1 in Depression","authors":"Hui Li,&nbsp;Chenju Yi","doi":"10.1111/apha.70198","DOIUrl":"10.1111/apha.70198","url":null,"abstract":"&lt;p&gt;Dysregulation of glutamatergic and GABAergic signaling in certain brain regions is a well-established pathological hallmark of many central nervous system (CNS) disorders [&lt;span&gt;1-3&lt;/span&gt;], with depression being a prime example [&lt;span&gt;4, 5&lt;/span&gt;]. The central amygdala (CeA) has emerged as a critical region in governing psychiatric health. Specifically, increased excitatory output from glutamatergic neurons or functional deficits in GABAergic inhibitory neurons within the CeA have been consistently linked to depressive-like behaviors in animal models [&lt;span&gt;6&lt;/span&gt;]. However, the upstream molecular mechanism that regulates the functional integrity of these distinct neuronal populations within the CeA remains unclear. Clarifying these pathways is therefore urgently needed, as it holds the key to identify novel therapeutic targets for restoring the fine balance between excitatory and inhibitory neurotransmitters that is essential for determining depressive behaviors.&lt;/p&gt;&lt;p&gt;A recent study in &lt;i&gt;Acta Physiologica&lt;/i&gt; titled “Cell type-specific loss of SIRT1 in central amygdala leads to depression-like behaviors by altering neuronal excitability in mice” [&lt;span&gt;7&lt;/span&gt;], Wang and colleagues identified Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD)&lt;sup&gt;+&lt;/sup&gt;-dependent histone deacetylase, as a key molecular regulator governing the activity of CeA neurons, revealing a dual role that is cell-type dependent. SIRT1 has been previously identified as a key molecule in regulating negative emotion such as depression in animal models, positioning it as a potential therapeutic target for alleviating depression-related pathology [&lt;span&gt;8&lt;/span&gt;]. However, given the functional heterogeneity of SIRT1 across different brain regions and cell types, the development of SIRT1-targeting interventions remains a critical challenge. Wang and colleagues previously demonstrated that SIRT1 in the CeA can mediate chronic pain-induced depression [&lt;span&gt;9&lt;/span&gt;], suggesting that CeA SIRT1 might serve as a key molecule involved in the development of depression. Therefore, understanding how SIRT1 affects different CeA neuronal subtypes is essential for refining therapeutic strategies to restore neuronal balance in depression.&lt;/p&gt;&lt;p&gt;The recent study by Wang and colleagues reveals that the function of SIRT1 in the CeA is highly cell-type dependent. Specifically, knocking down SIRT1 in CeA glutamatergic neurons directly increases their activity, leading to hyperexcitability and subsequent depressive-like behaviors. In contrast, knocking down SIRT1 in GABAergic neurons produces a dual effect: it not only reduces the inhibitory output of GABAergic neurons but also indirectly increases the activity of glutamatergic neurons. Together, these findings establish that the disruption of excitatory and inhibitory output within the CeA is a key mechanism underlying depression, highlighting SIRT1 as a cell type specific regulator of neuronal activity. Such findings provide ","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apha.70198","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147429510","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":"Reciprocal Adipose-Heart Regulation of NRAC","authors":"Zhiyao Fu,&nbsp;Chao Zhang,&nbsp;Ren Zhang","doi":"10.1111/apha.70197","DOIUrl":"10.1111/apha.70197","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147388947","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":"Salivary IL-6 Shows Greater Intraindividual Stability Than Other Stress-Related Cytokines in Young Adults","authors":"Lea Vuletić,&nbsp;Stjepan Špalj,&nbsp;Ivana Lapić,&nbsp;Blaženka Ladika Davidović,&nbsp;Petra Šimičić,&nbsp;Jasmina Šipkar,&nbsp;Ivan Šamija,&nbsp;Dunja Rogić,&nbsp;Iva Z. Alajbeg","doi":"10.1111/apha.70191","DOIUrl":"10.1111/apha.70191","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147375384","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":"Physical Inactivity Drives COPD Progression Beyond Airflow Limitation","authors":"Salvatore Fuschillo,&nbsp;Claudio Candia,&nbsp;Pasquale Ambrosino,&nbsp;Carmen Lombardi,&nbsp;Claudia Merola,&nbsp;Giuseppe Rengo,&nbsp;Mauro Maniscalco","doi":"10.1111/apha.70192","DOIUrl":"10.1111/apha.70192","url":null,"abstract":"","PeriodicalId":107,"journal":{"name":"Acta Physiologica","volume":"242 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147375440","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}