Fatima Maqoud

Scopus Publications

Actions of Midostaurin as Cation Channel and Tyrosine Kinase Inhibitor in Diffuse Intrinsic Pontine Glioma Cell Lines
Marina Antonacci, Annamaria Di Turi, Morena Miciaccia, Michele Denora, Fatima Maqoud, et al.
Cancers, 2026
Tyrosine kinases (TKs) are drug targets in diffuse intrinsic pontine glioma (DIPG). Ion channels are emerging targets in cancer. TKIs targeting different kinases such as everolimus, crizotinib, dasatinib, erlotinib, lapatinib, perifosine and midostaurin (0.001–100 μM) were investigated on cell proliferation and ion channel currents. Methods: Cell viability assays in parallel with a patch-clamp study and Western blot of target proteins are performed in SU-DIPG-36 and SU-DIPG-50 cells. Results: Midostaurin is the most effective drug in different assays. Patch-clamp investigations show that the application of midostaurin reduced the inward and outward whole-cell cation channel currents vs. controls in the presence of low internal ATP. These currents were sensitive to the KATP channel inhibitors glibenclamide and repaglinide and were fully reduced by the unselective blocker TEA-BaCl2. Midostaurin also reduced currents that are sensitive to TRPV1 channel blockers capsazepine and ruthenium-red. The IC50 values of midostaurin as an antiproliferative drug and ion channel inhibitor in either cell line are in the sub-micromolar range. In SU-DIPG-36 cells midostaurin causes a concentration-dependent upregulation of autophagy markers. Conclusions: The inhibition of cation channel currents by midostaurin in SU-DIPG-36 and SU-DIPG-50 cells and the autophagy potentiation in SU-DIPG-36 cells can be novel mechanisms in DIPG.
Modulation of KATP channels by diazoxide preserves mitochondrial function and barrier integrity under staurosporine-induced epithelial stress
Fatima Maqoud, Eleonora Malerba, Simona Drago, Antonella Orlando, Domenica Mallardi, et al.
British Journal of Pharmacology, 2026
Background and Purpose Intestinal barrier dysfunction caused by mitochondrial stress, oxidative damage and apoptosis, are hallmarks of dysbiosis‐associated gastrointestinal (GI) disorders. Staurosporine causes downstream features of dysbiosis‐induced epithelial damage. K ATP (K ir 6.x) channels act as metabolic sensors linking cellular energetics to stress adaptation. We investigated whether diazoxide preserved epithelial integrity under staurosporine‐induced stress. Experimental Approach HCEC‐1CT cells were exposed to staurosporine or in combination with diazoxide. Mitochondrial function, ROS generation, transepithelial electrical resistance (TEER), paracellular permeability, tight junction expression, K ATP channel subunit regulation, MAPK signalling and epigenetic markers were assessed using functional assays, RT‐qPCR and western blotting. K ATP channel involvement was validated using the blocker glibenclamide. Key Results Diazoxide restored mitochondrial function following staurosporine‐induced damage in the co‐treatment model, with an EC50 of 6 × 10 −5 M. Reducing ROS accumulation and preserving epithelial barrier integrity, as demonstrated by maintenance of TEER and paracellular sealing. Diazoxide enhanced SUR1/SUR2 expression and glycosylation, preserved ERK1/2 phosphorylation and sustained histone H3 lysine 27 acetylation, supporting active gene transcription under stress. Co‐administration with staurosporine prevented downregulation of K ATP channel subunits. Diazoxide also attenuated staurosporine‐induced dysregulation of pro‐inflammatory and apoptotic genes, reinforcing its function as a molecular stabilizer under cytotoxic stress. These protective effects were reversed by glibenclamide, indicating K ATP channel dependence. Conclusions and Implications Diazoxide may be a potential therapeutic candidate for oxidative stress–driven barrier dysfunction in gastrointestinal diseases. Future studies incorporating physiologically relevant stressors, such as LPS or H₂S, will be important to validate these protective mechanisms in contexts more directly related to microbial dysbiosis.
Lactobacillus rhamnosus GG and Lactobacillus paracasei IMPC2.1 Mitigate LPS-Induced Epithelial Barrier Dysfunction: A Focus on Autophagy Regulation
Antonella Orlando, Fatima Maqoud, Domenica Mallardi, Simona Drago, Eleonora Malerba, et al.
International Journal of Molecular Sciences, 2025
The intestinal epithelial barrier is critical for maintaining gut homeostasis, yet its integrity can be compromised by inflammation and microbial dysbiosis. Here, we demonstrate that Lactobacillus rhamnosus GG (LGG) and Lactobacillus paracasei IMPC2.1 (L. paracasei) show their effectiveness in enhancing epithelial barrier function and modulating autophagy, counteract the epithelial barrier dysfunction, induced by Lipopolysaccharide (LPS), in Caco-2 cells by modulating tight junction (TJ) protein expression through regulation of inflammation and apoptosis. LPS exposure significantly reduced transepithelial electrical resistance (TEER) and increased paracellular permeability, effects that were partially reversed by both probiotic strains. Western blot analysis revealed that LPS downregulated ZO-1, Occludin, and p-mTOR, while upregulating autophagy markers LC3-II and Beclin1, without affecting p62 levels. The latter finding indicated an impairment of autophagy flux, confirmed by immunofluorescence experiments. Co-treatment with LGG or L. paracasei restored TJ protein expression and alleviated the LPS-induced impairment of autophagic flux. Both probiotics suppressed LPS-induced cyclooxygenase-2 (Cox-2) and Bax upregulation, suggesting anti-inflammatory and anti-apoptotic effects. In the complex interplay between inflammation, autophagy, and apoptosis, these findings highlight a key regulatory mechanism in probiotic-mediated epithelial protection, underscoring the therapeutic potential of LGG and L. paracasei in mitigating gut barrier dysfunction.
Ion Channel–Extracellular Matrix Interplay in Colorectal Cancer: A Network-Based Approach to Tumor Microenvironment Remodeling
Alberta Terzi, Fatima Maqoud, Davide Guido, Domenica Mallardi, Michelangelo Aloisio, et al.
International Journal of Molecular Sciences, 2025
The progression of colorectal cancer (CRC) is driven by dynamic interactions between tumor cells and their microenvironment, particularly the extracellular matrix (ECM). Ion channels, critical regulators of cellular signaling, have emerged as mediators of ECM remodeling and tumor aggressiveness. In this study, we integrate transcriptomic data from 185 CRC tumors and 157 adjacent normal tissues with network modeling to dissect the interplay between ion channels and the ECM. We identified 4036 differentially expressed genes (DEGs), including 188 ion channel-associated DEGs (IC-DEGs) enriched in ECM-related pathways, such as collagen assembly, matrix metalloproteinase regulation, and mechanotransduction. Structural equation modeling revealed an active CRC−ion channel module (CRC-IC) comprising 482 nodes and 422 edges, highlighting dysregulated interactions between ECM components (e.g., COL1A1, COL5A2, VCAN, LAMA4, LA-MA5, LAMC1), ion channels (e.g., TRPM5 and SLC16A1), and cytoskeletal regulators. Key nodes, including CHST11 and VCAN, were associated with ECM sulfation, tumor invasiveness, and immune evasion. Notably, survival was associated with MAPK1, SLC16A1, and ABCB4 in relation to patient prognosis. Our findings underscore the pivotal role of ion channels as co-factors in ECM dynamics in CRC, offering mechanistic insights into tumor-stroma crosstalk and identifying potential therapeutic targets to disrupt microenvironment-driven progression.
The Dual Role of Exogenous Hydrogen Sulfide (H2S) in Intestinal Barrier Mitochondrial Function: Insights into Cytoprotection and Cytotoxicity Under Non-Stressed Conditions
Domenica Mallardi, Guglielmina Chimienti, Fatima Maqoud, Antonella Orlando, Simona Drago, et al.
Antioxidants, 2025
Hydrogen sulfide (H2S) is a critical gasotransmitter that plays a dual role in physiological and pathological processes, particularly in the gastrointestinal tract. While physiological levels of H2S exert cytoprotective effects, excessive concentrations can lead to toxicity, oxidative stress, and inflammation. The aim of this study was to investigate the dose-dependent effects of exogenous H2S on mitochondrial functions and biogenesis in intestinal epithelial cells under non-stressed conditions. Using a Caco-2 monolayer model, we evaluated the impact of sodium hydrosulfide (NaHS) at concentrations ranging from 1 × 10−7 M to 5 × 10−3 M on mitochondrial metabolism, redox balance, antioxidant defense, inflammatory responses, autophagy/mitophagy, and apoptosis. Our results demonstrated a biphasic response: low-to-moderate H2S concentrations (1 × 10−7 M–1.5 × 10−3 M) enhance mitochondrial biogenesis through PGC-1α activation, upregulating TFAM and COX-4 expression, and increasing the mtDNA copy number. In contrast, higher concentrations (2 × 10−3–5 × 10−3 M) impair mitochondrial function, induce oxidative stress, and promote apoptosis. These effects are associated with elevated reactive oxygen species (ROS) production, dysregulation of antioxidant enzymes, and COX-2-mediated inflammation. H2S-induced autophagy/mitophagy is a protective mechanism at intermediate concentrations but fails to mitigate mitochondrial damage at toxic levels. This study underscores the delicate balance between the cytoprotective and cytotoxic effects of exogenous H2S in intestinal cells, helping to develop new therapeutic approaches for gastrointestinal disorders.
Mapping Research Trends on Intestinal Permeability in Irritable Bowel Syndrome with a Focus on Nutrition: A Bibliometric Analysis
Domenica Mallardi, Fatima Maqoud, Davide Guido, Michelangelo Aloisio, Michele Linsalata, et al.
Nutrients, 2025
Irritable Bowel Syndrome (IBS) is a complex gastrointestinal disorder characterized by chronic abdominal pain and altered bowel habits, often linked to disruptions in intestinal barrier function. Increased intestinal permeability plays a key role in IBS pathogenesis, affecting immune responses, gut microbiota, and inflammation. This study conducts a bibliometric analysis to explore global research trends on intestinal permeability in IBS, focusing on key contributors, collaboration networks, and thematic shifts, particularly the interplay between the intestinal barrier, gut microbiota, and dietary components. A total of 411 articles were retrieved from Scopus, with 232 studies analyzed using Bibliometrix in R. To optimize screening, ASReview, a machine learning tool, was employed, utilizing the Naïve Bayes algorithm combined with Term Frequency-Inverse Document Frequency (TF-IDF) for adaptive ranking of articles by relevance. This approach significantly improved screening step efficacy. The analysis highlights growing research interest, with China and the USA as leading contributors. Key themes include the role of gut microbiota in modulating permeability, the impact of dietary components (fiber, probiotics, bioactive compounds) on tight junction integrity, and the exploration of therapeutic agents. Emerging studies suggest integrating gut barrier modulation with nutritional and microbiome-targeted strategies for IBS management. This study provides a comprehensive overview of research on intestinal permeability in IBS, mapping its evolution and identifying major trends. By highlighting key contributors and thematic areas, it offers insights to guide future investigations into the interplay between gut permeability, diet, and microbiota, advancing understanding of IBS pathophysiology and management.
KATP Channel Inhibitors Reduce Cell Proliferation Through Upregulation of H3K27ac in Diffuse Intrinsic Pontine Glioma: A Functional Expression Investigation
Marina Antonacci, Fatima Maqoud, Annamaria Di Turi, Morena Miciaccia, Maria Grazia Perrone, et al.
Cancers, 2025
Background: Diffuse intrinsic pontine glioma [DIPG] is a fatal pediatric disease characterized by a post-translational modification, a replacement of lysine by methionine in position 27 of the N-terminal [H3K27M] tail of histone 3 isoform-1 [H3.1] or histone 3 isoform-3 [H3.3], respectively, expressed in the DIPG-36 and DIPG-50 cells. We investigated the role of cation channels in DIPG cells for the first time and the effects of ATP-sensitive K+[KATP] and TRPV1 channel modulators. Methods: Experiments were performed using “in vitro” cytotoxic assays combined with the patch clamp technique, RT-PCR, Western blot, and flow cytometry assays. Results: The most effective anti-proliferative drugs were repaglinide and glibenclamide after short and long-term incubation [6–96 h]. These drugs reduced macroscopic currents of the DIPG cells recorded in whole-cell patch clamp. Repaglinide concentration dependently enhanced the target protein H3K27ac in Western blotting after 48 h of incubation. This drug reduced cell diameter and enhanced cleaved caspase-3 in DIPG cells; total AKT/mTOR levels and phospho-mTOR were downregulated in DIPG-36. Conclusions: KATP and TRPV1 channels are functionally expressed, and sulphonylureas are effective antiproliferative upregulating H3K27ac with apoptosis in DIPG cells and the sub-micromolar concentrations in DIPG-50.
Gain-of-function mutations in KATP channel subunits compromise colonic tight junction integrity and epithelial homeostasis in murine models of Cantú syndrome
Fatima Maqoud, Domenica Mallardi, Antonella Orlando, Domenico Tricarico, Colin G. Nichols, et al.
Frontiers in Medicine, 2025
IntroductionCantú syndrome (CS) is a rare genetic disorder caused by gain-of-function (GOF) mutations in the KCNJ8 (Kir6.1) or ABCC9 (SUR2) subunits of ATP-sensitive potassium (KATP) channels. CS is characterized by multisystem abnormalities such as cardiovascular defects, hypertrichosis, and skeletal malformations, but its impact on intestinal homeostasis remains poorly understood.MethodsWe investigated the effects of CS-associated KATP channel overactivity on epithelial barrier integrity and tight junction (TJ) proteins using murine models. Heterozygous (SUR2wt/AV) and homozygous (SUR2AV/AV) SUR2(A478V) mutants, as well as Kir6.1(V65M) mice, were studied. mRNA and protein expression of Occludin, Claudin-1, and ZO-1 were analyzed, alongside histological and immunohistochemical assessments. Markers of apoptosis and survival, including caspase-3 activity and BCL2/BCL2L1 expression, were also evaluated.ResultsGOF mutations in KATP channels caused significant dysregulation of TJ proteins. Occludin expression was increased in SUR2AV/AV mice but decreased in SUR2wt/AV and Kir6.1 mutants, while Claudin-1 and ZO-1 were consistently reduced across all models. Immunohistochemistry revealed disrupted TJ localization and reduced apical junctional integrity. Histological analyzes showed epithelial disorganization, smooth muscle hypertrophy, fibrosis, and inflammatory infiltration. These alterations were accompanied by increased caspase-3 activity and reduced BCL2 and BCL2L1 expression.DiscussionOur findings demonstrate that CS-associated KATP channel GOF mutations disrupt tight junction dynamics and induces structural remodeling of the colon. This establishes a novel link between KATP channel dysregulation, metabolic-epithelial interactions, and intestinal pathophysiology in CS. Furthermore, the results highlight potential therapeutic targets to mitigate barrier dysfunction, providing a basis for developing interventions to address gastrointestinal symptoms in CS.
Role of Increasing Body Mass Index in Gut Barrier Dysfunction, Systemic Inflammation, and Metabolic Dysregulation in Obesity
Nutrients, 2025
Transcriptomic Module Discovery of Diarrhea-Predominant Irritable Bowel Syndrome: A Causal Network Inference Approach
Davide Guido, Fatima Maqoud, Michelangelo Aloisio, Domenica Mallardi, Blendi Ura, et al.
International Journal of Molecular Sciences, 2024
Irritable bowel syndrome with diarrhea (IBS-D) is the most prevalent subtype of IBS, characterized by chronic gastrointestinal symptoms in the absence of identifiable pathological findings. This study aims to investigate the molecular mechanisms underlying IBS-D using transcriptomic data. By employing causal network inference methods, we identify key transcriptomic modules associated with IBS-D. Utilizing data from public databases and applying advanced computational techniques, we uncover potential biomarkers and therapeutic targets. Our analysis reveals significant molecular alterations that affect cellular functions, offering new insights into the complex pathophysiology of IBS-D. These findings enhance our understanding of the disease and may foster the development of more effective treatments.
The Functional Interaction of KATP and BK Channels with Aquaporin-4 in the U87 Glioblastoma Cell
Fatima Maqoud, Laura Simone, Domenico Tricarico, Giulia Maria Camerino, Marina Antonacci, et al.
Biomedicines, 2024
Role of Extracellular Vesicles in Crohn’s Patients on Adalimumab Who Received COVID-19 Vaccination
Maria De Luca, Biagia Musio, Francesco Balestra, Valentina Arrè, Roberto Negro, et al.
International Journal of Molecular Sciences, 2024
Anti-Inflammatory Effects of a Novel Acetonitrile–Water Extract of Lens Culinaris against LPS-Induced Damage in Caco-2 Cells
Fatima Maqoud, Antonella Orlando, Domenico Tricarico, Marina Antonacci, Annamaria Di Turi, et al.
International Journal of Molecular Sciences, 2024
Effect of a 12-Week Walking Program Monitored by Global Physical Capacity Score (GPCS) on Circulating Cell-Free mtDNA and DNase Activity in Patients with Irritable Bowel Syndrome
Guglielmina Chimienti, Francesco Russo, Antonella Bianco, Fatima Maqoud, Caterina De Virgilio, et al.
International Journal of Molecular Sciences, 2024
The Role of Ion Channels in Functional Gastrointestinal Disorders (FGID): Evidence of Channelopathies and Potential Avenues for Future Research and Therapeutic Targets
Fatima Maqoud, Domenico Tricarico, Rosanna Mallamaci, Antonella Orlando, Francesco Russo
International Journal of Molecular Sciences, 2023
Zoledronic Acid Blocks Overactive Kir6.1/SUR2-Dependent KATP Channels in Skeletal Muscle and Osteoblasts in a Murine Model of Cantú Syndrome
Rosa Scala, Fatima Maqoud, Conor McClenaghan, Theresa M. Harter, Maria Grazia Perrone, et al.
Cells, 2023
Molecular Composition and Biological Activity of a Novel Acetonitrile–Water Extract of Lens Culinaris Medik in Murine Native Cells and Cell Lines Exposed to Different Chemotherapeutics Using Mass Spectrometry
Annamaria Di Turi, Marina Antonacci, Jacopo Raffaele Dibenedetto, Fatima Maqoud, Francesco Leonetti, et al.
Cells, 2023
Immunohistochemical, pharmacovigilance, and omics analyses reveal the involvement of ATP-sensitive K+ channel subunits in cancers: role in drug–disease interactions
Fatima Maqoud, Nicola Zizzo, Marcella Attimonelli, Antonella Tinelli, Giuseppe Passantino, et al.
Frontiers in Pharmacology, 2023
β3 Adrenergic Receptor Agonist Mirabegron Increases AQP2 and NKCC2 Urinary Excretion in OAB Patients: A Pleiotropic Effect of Interest for Patients with X-Linked Nephrogenic Diabetes Insipidus
Serena Milano, Fatima Maqoud, Monica Rutigliano, Ilenia Saponara, Monica Carmosino, et al.
International Journal of Molecular Sciences, 2023
Counteractions of a Novel Hydroalcoholic Extract from Lens Culinaria against the Dexamethasone-Induced Osteoblast Loss of Native Murine Cells
Marina Antonacci, Jacopo Raffaele Dibenedetto, Fatima Maqoud, Gerardo Centoducati, Nicola Colonna, et al.
Cells, 2022
Bisphosphonates Targeting Ion Channels and Musculoskeletal Effects
Rosa Scala, Fatima Maqoud, Marina Antonacci, Jacopo Raffaele Dibenedetto, Maria Grazia Perrone, et al.
Frontiers in Pharmacology, 2022
ATP-sensitive Potassium Channel Subunits in Neuroinflammation: Novel Drug Targets in Neurodegenerative Disorders
Fatima Maqoud, Rosa Scala, Malvina Hoxha, Bruno Zappacosta, Domenico Tricarico
CNS and Neurological Disorders Drug Targets, 2022
Multicenter Observational/Exploratory Study Addressed to the Evaluation of the Effectiveness and Safety of Pharmacological Therapy in Opioid-Dependent Patients in Maintenance Therapy in Southern Italy
Fatima Maqoud, Giada Fabio, Nunzio Ciliero, Marina Antonacci, Francesca Mastrangelo, et al.
Pharmaceutics, 2022
Zoledronic acid as a novel dual blocker of KIR6.1/2-SUR2 subunits of ATP-sensitive K+ channels: Role in the adverse drug reactions
Fatima Maqoud, Rosa Scala, Vincenzo Tragni, Ciro Leonardo Pierri, Maria Grazia Perrone, et al.
Pharmaceutics, 2021
Consequences of sur2[a478v] mutation in skeletal muscle of murine model of cantu syndrome
Rosa Scala, Fatima Maqoud, Nicola Zizzo, Giuseppe Passantino, Antonietta Mele, et al.
Cells, 2021
Oxtr/TRPV1 expression and acclimation of skeletal muscle to cold-stress in male mice
Elena Conte, Adele Romano, Michela De Bellis, Marialuisa de Ceglia, Maria Rosaria Carratù, et al.
Journal of Endocrinology, 2021
Bridging repair of the abdominal wall in a rat experimental model. Comparison between uncoated and polyethylene oxide-coated equine pericardium meshes
Alessandro Pasculli, Angela Gurrado, Giuseppe Massimiliano De Luca, Antonietta Mele, Andrea Marzullo, et al.
Scientific Reports, 2020
Pathophysiological Consequences of KATP Channel Overactivity and Pharmacological Response to Glibenclamide in Skeletal Muscle of a Murine Model of Cantù Syndrome
Rosa Scala, Fatima Maqoud, Nicola Zizzo, Antonietta Mele, Giulia Maria Camerino, et al.
Frontiers in Pharmacology, 2020
The hydroxypropyl-β-cyclodextrin-minoxidil inclusion complex improves the cardiovascular and proliferative adverse effects of minoxidil in male rats: Implications in the treatment of alopecia
Fatima Maqoud, Nicola Zizzo, Antonietta Mele, Nunzio Denora, Giuseppe Passantino, et al.
Pharmacology Research and Perspectives, 2020
Thymidine Phosphorylase Expression and Microvascular Density Correlation Analysis in Canine Mammary Tumor: Possible Prognostic Factor in Breast Cancer
Nicola Zizzo, Giuseppe Passantino, Roberta Maria D'alessio, Antonella Tinelli, Giuseppe Lopresti, et al.
Frontiers in Veterinary Science, 2019
Zoledronic acid modulation of TRPV1 channel currents in osteoblast cell line and native rat and mouse bone marrow-derived osteoblasts: Cell proliferation and mineralization effect
Rosa Scala, Fatima Maqoud, Mariacristina Angelelli, Ramon Latorre, Maria Perrone, et al.
Cancers, 2019
Single-dose extended-toxicity preclinical study on novel radiotracer formulations for use in the diagnosis of neuroendocrine tumor and neurodegenerative disorders
Current Topics in Pharmacology, 2019
Cell cycle regulation by Ca2+-activated K+ (BK) channels modulators in SH-SY5Y neuroblastoma cells
Fatima Maqoud, Angela Curci, Rosa Scala, Alessandra Pannunzio, Federica Campanella, et al.
International Journal of Molecular Sciences, 2018
Alginate-Based Hydrogel Containing Minoxidil/Hydroxypropyl-β-Cyclodextrin Inclusion Complex for Topical Alopecia Treatment
Angela Lopedota, Nunzio Denora, Valentino Laquintana, Annalisa Cutrignelli, Antonio Lopalco, et al.
Journal of Pharmaceutical Sciences, 2018
Characterization of minoxidil/hydroxypropyl-β-cyclodextrin inclusion complex in aqueous alginate gel useful for alopecia management: Efficacy evaluation in male rat
Domenico Tricarico, Fatima Maqoud, Angela Curci, Giuliamaria Camerino, Nicola Zizzo, et al.
European Journal of Pharmaceutics and Biopharmaceutics, 2018
Molecular structure and function of big calcium-activated potassium channels in skeletal muscle: Pharmacological perspectives
Fatima Maqoud, Michela Cetrone, Antonietta Mele, Domenico Tricarico
Physiological Genomics, 2017
A novel injectable formulation of 6-fluoro-L-DOPA imaging agent for diagnosis of neuroendocrine tumors and Parkinson's disease
Adriana Trapani, Domenico Tricarico, Antonietta Mele, Fatima Maqoud, Delia Mandracchia, et al.
International Journal of Pharmaceutics, 2017
From Morocco to Italy: How women’s bodies reflect their change of residence
Collegium Antropologicum, 2016
Antiproliferative effects of neuroprotective drugs targeting big Ca2+-activated K+ (BK) channel in the undifferentiated neuroblastoma cells
Current Topics in Pharmacology, 2016
ATP sensitive potassium channels in the skeletal muscle function: Involvement of the KCNJ11(Kir6.2) gene in the determination of mechanical warner bratzer shear force
Domenico Tricarico, Maria Selvaggi, Giuseppe Passantino, Pasquale De Palo, Cataldo Dario, et al.
Frontiers in Physiology, 2016