HIF-1α and HIF-2α differentially regulate alveolar macrophage maturation and function Elena Priego, Irene Adan-Barrientos, Ruth Conde-Garrosa, Sarai Martínez-Cano, Iria Sánchez, Diego Mañanes, Annalaura Mastrangelo, Joaquín Amores-Iniesta, Helena M. Izquierdo, David Sancho Cell Reports, 2026 Alveolar macrophages (AMs) reside in the oxygen-rich alveoli, where hypoxia-inducible transcription factor (HIF) subunits are targeted for degradation by the Von Hippel-Lindau protein (pVHL). We previously showed that Vhl-deficient AMs are immature and functionally impaired. Here, we define isoform-specific roles of HIF-1α and HIF-2α in the regulation of AM maturation and function. Expression of either isoform alone is sufficient to intrinsically, and differentially, impair AM terminal maturation and self-renewal, with complete rescue observed only when both HIF-1α and HIF-2α are deleted in Vhl-deficient AMs. HIF-1α drives glycolytic reprogramming in AMs, while HIF-2α disrupts fatty acid oxidation and surfactant clearance. Consequently, HIF-2α stabilization limits the capacity of AMs to resolve surfactant excess in a mouse model of pulmonary alveolar proteinosis, indicating HIF-2α as a potential therapeutic target. Overall, HIF inactivation ensures optimal AM maturation and metabolic adaptation to the high-oxygen alveolar niche, revealing non-redundant functional specificities of each HIF-α isoform.
Mitochondrial metabolism regulates the immunogenic responsiveness of dendritic cells Ignacio Heras-Murillo, Diego Mañanes, Josep Calafell-Segura, Adrián Belinchón García, Clara Borràs-Eroles, Pablo Munné, Annalaura Mastrangelo, Sarai Martínez-Cano, Pablo Hernansanz-Agustín, María A. Zuriaga, José J. Fuster, Marten Szibor, Ignacio Melero, José Antonio Enríquez, Navdeep S. Chandel, Esteban Ballestar, Stefanie K. Wculek, David Sancho Cell Metabolism, 2026
A high-fat diet nutritional intervention reprograms cardiac metabolism and improves systolic function in a pig model of heart failure with reduced ejection fraction Carlos Galán-Arriola, Daniel Pérez-Camargo, Alessia Ferrarini, Annalaura Mastrangelo, María Isabel Higuero-Verdejo, Gonzalo Javier López-Martín, Ana Devesa, Rocío Villena Gutiérrez, Miguel Fernández-Tocino, Anabel Díaz-Guerra, Lourdes Montero-Cruces, Manuel Carnero, Rodrigo Fernández-Jiménez, Valentin Fuster, Javier Sánchez-González, Borja Ibáñez Basic Research in Cardiology, 2026 Most forms of heart failure are characterized by a metabolic switch from the use of fatty acids to glucose as the main fuel source for ATP generation in the myocardium. Whether metabolic reprogramming is a therapeutic target remains controversial. In this study, heart failure with reduced ejection fraction (HFrEF) and metabolic switch (i.e., increased myocardial glucose uptake) was induced in pigs by generating viable dysfunctional myocardium secondary to progressive coronary artery stenosis. Pigs ( n = 19) were then randomized to a high-fat diet (HFD, chow diet supplemented with 20% lard) or control diet (no supplementation) for two months. Pre- and post-nutritional treatment contrast-enhanced cardiac magnetic resonance (CMR) and 18 FDG-PET/CT studies were performed. Hearts were then harvested for further analysis. LVEF significantly improved in pigs receiving the 2-month HFD (38% [33, 43] to 54% [47, 62], p = 0.036) but remained unchanged in control-diet pigs (36% [35, 45] to 41% [38, 43], p = 0.24). HFD-fed pigs had a smaller extent of fibrosis after the dietary intervention (late gadolinium enhancement 0.45% LV [0.17, 1.67] vs 6.23 [5.54, 9.57], p = 0.0047). On 18 FDG-PET, a reversion of the metabolic reprogramming in the LAD-dysfunctional myocardium was observed only in HFD-fed pigs (0.46 counts [0.21, 0.65] vs 1.80 [1.53, 2.83], p = 0.016). Transmission electron microscopy of explanted hearts revealed less fragmented mitochondrial and a lower lipid droplet density in cardiomyocytes from HFD-fed pigs (38 per 10 µm3 [34, 50] vs 96 [78, 124], p = 0.022), and this was accompanied by increased expression of genes involved in fatty acid metabolism and downregulation of genes encoding glucose import proteins. In conclusion, in a large animal model of HFrEF secondary to myocardial dysfunction with a metabolic switch, a nutritional intervention based on HFD feeding was associated with a cardiac metabolic restoration of fatty acid substrate use, restoration of cardiomyocyte lipid trafficking and significantly improved systolic function.
Mitochondrial complex I activity promotes antigen cross-presentation in dendritic cells Sofía C. Khouili, Elena Priego, Ignacio Heras-Murillo, Gillian Dunphy, Annalaura Mastrangelo, Sarai Martínez-Cano, Vanessa Nuñez, Manuel Rodrigo-Tapias, Adrián Belinchón-García, Johan Garaude, Salvador Iborra, Navdeep S. Chandel, Patricia González-Rodríguez, Michel Enamorado, David Sancho Science Immunology, 2026 Mitochondrial metabolism modulates immune cell signaling, yet how individual electron transport chain complexes fine-tune dendritic cell (DC) function remains unclear. Here, we identify mitochondrial complex I (CI) as a critical metabolic checkpoint controlling antigen cross-presentation by DCs in mice. Deficiency of the CI subunit NDUFS4 in DCs led to the formation of a nonfunctional CI subcomplex, resulting in mildly impaired mitochondrial respiration without triggering a compensatory glycolytic shift. NDUFS4 deficiency limited endosomal escape of internalized antigens, thereby impairing antigen cross-presentation while largely preserving direct presentation. CI dysfunction lowered the NAD + /NADH ratio, concomitant with decreased ATP levels, and diminished neutral lipid storage and lipid peroxidation. Restoration of the NAD + /NADH ratio rescued cross-presentation in NDUFS4-deficient DCs. NDUFS2-deficient DCs showed similar defects in cross-presentation, which were also rescued by rebalancing the NAD + /NADH ratio. Together, these findings reveal a link between mitochondrial CI integrity, NAD + -driven redox metabolism, and antigen cross-presentation.
Imidazole propionate is a driver and therapeutic target in atherosclerosis Annalaura Mastrangelo, Iñaki Robles-Vera, Diego Mañanes, Miguel Galán, Marcos Femenía-Muiña, Ana Redondo-Urzainqui, Rafael Barrero-Rodríguez, Eleftheria Papaioannou, Joaquín Amores-Iniesta, Ana Devesa, Manuel Lobo-González, Alba Carreras, Katharina R. Beck, Sophie Ivarsson, Anders Gummesson, Georgios Georgiopoulos, Manuel Rodrigo-Tapias, Sarai Martínez-Cano, Ivan Fernández-López, Vanessa Nuñez, Alessia Ferrarini, Naohiro Inohara, Kimon Stamatelopoulos, Alberto Benguría, Danay Cibrian, Francisco Sánchez-Madrid, Vanesa Alonso-Herranz, Ana Dopazo, Coral Barbas, Jesús Vázquez, Juan Antonio López, Alicia González-Martín, Gabriel Nuñez, Konstantinos Stellos, Göran Bergström, Fredrik Bäckhed, Valentín Fuster, Borja Ibañez, David Sancho Nature, 2025 Atherosclerosis is the main underlying cause of cardiovascular diseases. Its prevention is based on the detection and treatment of traditional cardiovascular risk factors1. However, individuals at risk for early vascular disease often remain unidentified2. Recent research has identified new molecules in the pathophysiology of atherosclerosis3, highlighting the need for alternative disease biomarkers and therapeutic targets to improve early diagnosis and therapy efficacy. Here, we observed that imidazole propionate (ImP), produced by microorganisms, is associated with the extent of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration to atherosclerosis-prone mice fed with chow diet was sufficient to induce atherosclerosis without altering the lipid profile, and was linked to activation of both systemic and local innate and adaptive immunity and inflammation. Specifically, we found that ImP caused atherosclerosis through the imidazoline-1 receptor (I1R, also known as nischarin) in myeloid cells. Blocking this ImP–I1R axis inhibited the development of atherosclerosis induced by ImP or high-cholesterol diet in mice. Identification of the strong association of ImP with active atherosclerosis and the contribution of the ImP–I1R axis to disease progression opens new avenues for improving the early diagnosis and personalized therapy of atherosclerosis. Imidazole propionate produced by gut microbiota is associated with atherosclerosis in mouse models and in humans, and causes the development of atherosclerosis through activation of the imidazoline-1 receptor in myeloid cells.
SGLT2i Therapy Prevents Anthracycline-Induced Cardiotoxicity in a Large Animal Model by Preserving Myocardial Energetics Danielle Medina-Hernández, Laura Cádiz, Annalaura Mastrangelo, Andrea Moreno-Arciniegas, Miguel Fernández Tocino, Alejandro A. Cueto Becerra, Anabel Díaz-Guerra Priego, Warren A. Skoza, María Isabel Higuero-Verdejo, Gonzalo Javier López-Martín, Claudia Pérez-Martínez, Antonio de Molina-Iracheta, María Caballero-Valderrama, Javier Sánchez-González, David Sancho, Valentin Fuster, Carlos Galán-Arriola, Borja Ibáñez Jacc Cardiooncology, 2025 BACKGROUND: Anthracycline-induced cardiotoxicity (AIC) is characterized by a disruption in myocardial metabolism. OBJECTIVES: The authors used a large animal model to test sodium-glucose cotransporter inhibitor therapy to prevent AIC. METHODS: Female large white pigs (n = 36) were used to identify the most translational AIC regimen: 6 triweekly intravenous doxorubicin injections (1.8 mg/kg each). Another group of 32 pigs were randomized (1:1:2) to doxorubicin plus empagliflozin 20 mg, doxorubicin plus empagliflozin 10 mg, or doxorubicin control. Pigs were serially examined using multiparametric cardiac magnetic resonance and magnetic resonance spectroscopy. At the end of the 21-week follow-up period, blood samples were obtained to measure myocardial metabolic substrate extraction, and the left ventricle was harvested and processed for analysis using metabolomics, transmission electron microscopy, mitochondrial respirometry, and histopathology. RESULTS: Final left ventricular ejection fraction (LVEF), the prespecified primary outcome, was significantly higher in pigs receiving 20 mg empagliflozin than in the doxorubicin control group (median 57.5% [Q1-Q3: 55.5%-60.3%] vs 47.0% [Q1-Q3: 40.8%-47.8%]; P = 0.027). Final LVEF in pigs receiving 10 mg empagliflozin was 51% (Q1-Q3: 46.5%-55.5%; P = 0.020 vs 20 mg empagliflozin). The incidence of AIC events was 0%, 50%, and 72% in the empagliflozin 20 mg, empagliflozin 10 mg, and doxorubicin control groups, respectively. Empagliflozin 20 mg treatment resulted in enhanced ketone body consumption by the myocardium, preserved magnetic resonance spectroscopy-measured cardiac energetics, and improved mitochondrial structure and function on transmission electron microscopy and respirometry. These changes were more modest with the 10-mg empagliflozin dose. CONCLUSIONS: Sodium-glucose cotransporter-2 inhibitor therapy with empagliflozin exerts a dose-dependent cardioprotective effect against AIC. The improved LVEF was accompanied by enhanced ketone body consumption, improved cardiac energetics, and preserved mitochondrial structure and function.
Poststroke Lung Infection by Opportunistic Commensal Bacteria Is Not Mediated by Their Expansion in the Gut Microbiota Laura Díaz-Marugan, Mattia Gallizioli, Leonardo Márquez-Kisinousky, Silvia Arboleya, Annalaura Mastrangelo, Francisca Ruiz-Jaén, Jordi Pedragosa, Climent Casals, Francisco Javier Morales, Sara Ramos-Romero, Sara Traserra, Carles Justicia, Miguel Gueimonde, Marcel Jiménez, Josep Lluís Torres, Xabier Urra, Ángel Chamorro, David Sancho, Clara G. de los Reyes-Gavilán, Francesc Miró-Mur, Anna M. Planas Stroke, 2023 BACKGROUND: Respiratory and urinary tract infections are frequent complications in patients with severe stroke. Stroke-associated infection is mainly due to opportunistic commensal bacteria of the microbiota that may translocate from the gut. We investigated the mechanisms underlying gut dysbiosis and poststroke infection. METHODS: Using a model of transient cerebral ischemia in mice, we explored the relationship between immunometabolic dysregulation, gut barrier dysfunction, gut microbial alterations, and bacterial colonization of organs, and we explored the effect of several drug treatments. RESULTS: Stroke-induced lymphocytopenia and widespread colonization of lung and other organs by opportunistic commensal bacteria. This effect correlated with reduced gut epithelial barrier resistance, and a proinflammatory sway in the gut illustrated by complement and nuclear factor-κB activation, reduced number of gut regulatory T cells, and a shift of gut lymphocytes to γδT cells and T helper 1/T helper 17 phenotypes. Stroke increased conjugated bile acids in the liver but decreased bile acids and short-chain fatty acids in the gut. Gut fermenting anaerobic bacteria decreased while opportunistic facultative anaerobes, notably Enterobacteriaceae, suffered an expansion. Anti-inflammatory treatment with a nuclear factor-κB inhibitor fully abrogated the Enterobacteriaceae overgrowth in the gut microbiota induced by stroke, whereas inhibitors of the neural or humoral arms of the stress response were ineffective at the doses used in this study. Conversely, the anti-inflammatory treatment did not prevent poststroke lung colonization by Enterobacteriaceae. CONCLUSIONS: Stroke perturbs homeostatic neuro-immuno-metabolic networks facilitating a bloom of opportunistic commensals in the gut microbiota. However, this bacterial expansion in the gut does not mediate poststroke infection.
Bone marrow activation in response to metabolic syndrome and early atherosclerosis Ana Devesa, Manuel Lobo-González, Juan Martínez-Milla, Belén Oliva, Inés García-Lunar, Annalaura Mastrangelo, Samuel España, Javier Sanz, José M Mendiguren, Hector Bueno, Jose J Fuster, Vicente Andrés, Antonio Fernández-Ortiz, David Sancho, Leticia Fernández-Friera, Javier Sanchez-Gonzalez, Xavier Rossello, Borja Ibanez, Valentin Fuster European Heart Journal, 2022
Microbiota Sensing by Mincle-Syk Axis in Dendritic Cells Regulates Interleukin-17 and -22 Production and Promotes Intestinal Barrier Integrity María Martínez-López, Salvador Iborra, Ruth Conde-Garrosa, Annalaura Mastrangelo, Camille Danne, Elizabeth R. Mann, Delyth M. Reid, Valérie Gaboriau-Routhiau, Maria Chaparro, María P. Lorenzo, Lara Minnerup, Paula Saz-Leal, Emma Slack, Benjamin Kemp, Javier P. Gisbert, Andrzej Dzionek, Matthew J. Robinson, Francisco J. Rupérez, Nadine Cerf-Bensussan, Gordon D. Brown, David Bernardo, Salomé LeibundGut-Landmann, David Sancho Immunity, 2019
Mitochondrial complex I activity promotes antigen cross-presentation in dendritic cells SC Khouili, E Priego, I Heras-Murillo, G Dunphy, A Mastrangelo, ... Science Immunology 11 (119), eaef0098 , 2026 2026
Mitochondrial metabolism regulates the immunogenic responsiveness of dendritic cells I Heras-Murillo, D Mañanes, J Calafell-Segura, AB García, ... Cell metabolism , 2026 2026 Citations: 1
A high-fat diet nutritional intervention reprograms cardiac metabolism and improves systolic function in a pig model of heart failure with reduced ejection fraction C Galán-Arriola, D Pérez-Camargo, A Ferrarini, A Mastrangelo, ... Basic Research in Cardiology, 1-19 , 2026 2026
ERC-funded proof of concept grant: targeting imidazoline 1-receptor in atherosclerosis A Mastrangelo, I Robles-Vera, D Sancho European Heart Journal, ehaf1122 , 2026 2026
HIF-1α and HIF-2α transcription factors differentially regulate lung alveolar macrophage function E Priego, I Adán-Barrientos, R Conde-Garrosa, S Martínez-Cano, ... bioRxiv, 2025.11. 25.690373 , 2025 2025
Imidazole propionate is a driver and therapeutic target in atherosclerosis A Mastrangelo, I Robles-Vera, D Mañanes, M Galán, M Femenía-Muiña, ... Nature 645 (8079), 254-261 , 2025 2025 Citations: 63
TurbOmics: a web-based platform for the analysis of metabolomics data using a multi-omics integrative approach R Barrero-Rodríguez, JM Rodríguez, T Naake, W Huber, ... bioRxiv, 2025.05. 09.653072 , 2025 2025 Citations: 2
SGLT2i therapy prevents anthracycline-induced cardiotoxicity in a large animal model by preserving myocardial energetics D Medina-Hernández, L Cádiz, A Mastrangelo, A Moreno-Arciniegas, ... Cardio Oncology 7 (2), 171-184 , 2025 2025 Citations: 23
Poststroke lung infection by opportunistic commensal bacteria is not mediated by their expansion in the gut microbiota L Díaz-Marugan, M Gallizioli, L Márquez-Kisinousky, S Arboleya, ... Stroke 54 (7), 1875-1887 , 2023 2023 Citations: 31
Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis SK Wculek, I Heras-Murillo, A Mastrangelo, D Mananes, M Galan, ... Immunity 56 (3), 516-530. e9 , 2023 2023 Citations: 285
TurboPutative: A web server for data handling and metabolite classification in untargeted metabolomics R Barrero-Rodríguez, JM Rodriguez, R Tarifa, J Vázquez, A Mastrangelo, ... Frontiers in molecular biosciences 9, 952149 , 2022 2022 Citations: 8
Bone marrow activation in response to metabolic syndrome and early atherosclerosis A Devesa, M Lobo-Gonzalez, J Martinez-Milla, B Oliva, I Garcia-Lunar, ... European heart journal 43 (19), 1809-1828 , 2022 2022 Citations: 76
Metabolism of tissue macrophages in homeostasis and pathology SK Wculek, G Dunphy, I Heras-Murillo, A Mastrangelo, D Sancho Cellular & molecular immunology 19 (3), 384-408 , 2022 2022 Citations: 503
Microbiota sensing by Mincle-Syk axis in dendritic cells regulates interleukin-17 and-22 production and promotes intestinal barrier integrity M Martinez-Lopez, S Iborra, R Conde-Garrosa, A Mastrangelo, C Danne, ... Immunity 50 (2), 446-461. e9 , 2019 2019 Citations: 248
Metabolomics changes in patients with PAPP-A2 deficiency in response to rhIGF1 treatment A Mastrangelo, GA Martos-Moreno, FJ Ruperez, JA Chowen, C Barbas, ... Growth Hormone & IGF Research 42, 28-31 , 2018 2018 Citations: 7
“Gear mechanism” of bariatric interventions revealed by untargeted metabolomics P Samczuk, M Luba, J Godzien, A Mastrangelo, HR Hady, J Dadan, ... Journal of pharmaceutical and biomedical analysis 151, 219-226 , 2018 2018 Citations: 40
Metabolomic Changes in Patients with PAPP-A2 Deficiency in Response to rhIGF1 Treatment A Mastrangelo, G Martos-Moreno, FJ Rupérez, J Chowen, C Barbas, ... HORMONE RESEARCH IN PAEDIATRICS 90, 86-86 , 2018 2018
Metabolomics allows the discrimination of the pathophysiological relevance of hyperinsulinism in obese prepubertal children GÁ Martos-Moreno, A Mastrangelo, V Barrios, A García, JA Chowen, ... International Journal of Obesity 41 (10), 1473-1480 , 2017 2017 Citations: 35
Discriminant biomarkers of acute respiratory distress syndrome associated to H1N1 influenza identified by metabolomics HPLC‐QTOF‐MS/MS platform A Ferrarini, L Righetti, MP Martínez, M Fernández‐López, A Mastrangelo, ... Electrophoresis 38 (18), 2341-2348 , 2017 2017 Citations: 17
Chronic diseases and lifestyle biomarkers identification by metabolomics A Mastrangelo, C Barbas Metabolomics: From Fundamentals to Clinical Applications, 235-263 , 2017 2017 Citations: 53
MOST CITED SCHOLAR PUBLICATIONS
Metabolism of tissue macrophages in homeostasis and pathology SK Wculek, G Dunphy, I Heras-Murillo, A Mastrangelo, D Sancho Cellular & molecular immunology 19 (3), 384-408 , 2022 2022 Citations: 503
Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis SK Wculek, I Heras-Murillo, A Mastrangelo, D Mananes, M Galan, ... Immunity 56 (3), 516-530. e9 , 2023 2023 Citations: 285
Microbiota sensing by Mincle-Syk axis in dendritic cells regulates interleukin-17 and-22 production and promotes intestinal barrier integrity M Martinez-Lopez, S Iborra, R Conde-Garrosa, A Mastrangelo, C Danne, ... Immunity 50 (2), 446-461. e9 , 2019 2019 Citations: 248
From sample treatment to biomarker discovery: A tutorial for untargeted metabolomics based on GC-(EI)-Q-MS A Mastrangelo, A Ferrarini, F Rey-Stolle, A Garcia, C Barbas Analytica chimica acta 900, 21-35 , 2015 2015 Citations: 220
Altered metabolic and stemness capacity of adipose tissue-derived stem cells from obese mouse and human LM Perez, A Bernal, B de Lucas, N San Martin, A Mastrangelo, A Garcia, ... PLoS One 10 (4), e0123397 , 2015 2015 Citations: 124
Metabolomics as a tool for drug discovery and personalised medicine. A review A Mastrangelo, E G Armitage, A García, C Barbas Current topics in medicinal chemistry 14 (23), 2627-2636 , 2014 2014 Citations: 95
Insulin resistance in prepubertal obese children correlates with sex-dependent early onset metabolomic alterations A Mastrangelo, GÁ Martos-Moreno, A García, V Barrios, FJ Rupérez, ... International Journal of Obesity 40 (10), 1494-1502 , 2016 2016 Citations: 79
Bone marrow activation in response to metabolic syndrome and early atherosclerosis A Devesa, M Lobo-Gonzalez, J Martinez-Milla, B Oliva, I Garcia-Lunar, ... European heart journal 43 (19), 1809-1828 , 2022 2022 Citations: 76
Imidazole propionate is a driver and therapeutic target in atherosclerosis A Mastrangelo, I Robles-Vera, D Mañanes, M Galán, M Femenía-Muiña, ... Nature 645 (8079), 254-261 , 2025 2025 Citations: 63
Chronic diseases and lifestyle biomarkers identification by metabolomics A Mastrangelo, C Barbas Metabolomics: From Fundamentals to Clinical Applications, 235-263 , 2017 2017 Citations: 53
New insight on obesity and adipose-derived stem cells using comprehensive metabolomics A Mastrangelo, MI Panadero, LM Pérez, BG Gálvez, A García, C Barbas, ... Biochemical Journal 473 (14), 2187-2203 , 2016 2016 Citations: 46
“Gear mechanism” of bariatric interventions revealed by untargeted metabolomics P Samczuk, M Luba, J Godzien, A Mastrangelo, HR Hady, J Dadan, ... Journal of pharmaceutical and biomedical analysis 151, 219-226 , 2018 2018 Citations: 40
Metabolomics allows the discrimination of the pathophysiological relevance of hyperinsulinism in obese prepubertal children GÁ Martos-Moreno, A Mastrangelo, V Barrios, A García, JA Chowen, ... International Journal of Obesity 41 (10), 1473-1480 , 2017 2017 Citations: 35
Poststroke lung infection by opportunistic commensal bacteria is not mediated by their expansion in the gut microbiota L Díaz-Marugan, M Gallizioli, L Márquez-Kisinousky, S Arboleya, ... Stroke 54 (7), 1875-1887 , 2023 2023 Citations: 31
SGLT2i therapy prevents anthracycline-induced cardiotoxicity in a large animal model by preserving myocardial energetics D Medina-Hernández, L Cádiz, A Mastrangelo, A Moreno-Arciniegas, ... Cardio Oncology 7 (2), 171-184 , 2025 2025 Citations: 23
Metabolomic evaluation of Mitomycin C and rapamycin in a personalized treatment of pancreatic cancer A Navarrete, EG Armitage, M Musteanu, A García, A Mastrangelo, R Bujak, ... Pharmacology research & perspectives 2 (6), e00067 , 2014 2014 Citations: 22
Discriminant biomarkers of acute respiratory distress syndrome associated to H1N1 influenza identified by metabolomics HPLC‐QTOF‐MS/MS platform A Ferrarini, L Righetti, MP Martínez, M Fernández‐López, A Mastrangelo, ... Electrophoresis 38 (18), 2341-2348 , 2017 2017 Citations: 17
TurboPutative: A web server for data handling and metabolite classification in untargeted metabolomics R Barrero-Rodríguez, JM Rodriguez, R Tarifa, J Vázquez, A Mastrangelo, ... Frontiers in molecular biosciences 9, 952149 , 2022 2022 Citations: 8
Metabolomics changes in patients with PAPP-A2 deficiency in response to rhIGF1 treatment A Mastrangelo, GA Martos-Moreno, FJ Ruperez, JA Chowen, C Barbas, ... Growth Hormone & IGF Research 42, 28-31 , 2018 2018 Citations: 7
TurbOmics: a web-based platform for the analysis of metabolomics data using a multi-omics integrative approach R Barrero-Rodríguez, JM Rodríguez, T Naake, W Huber, ... bioRxiv, 2025.05. 09.653072 , 2025 2025 Citations: 2