José M. Mateos

766 total citations
18 papers, 517 citations indexed

About

José M. Mateos is a scholar working on Endocrine and Autonomic Systems, Pediatrics, Perinatology and Child Health and Surgery. According to data from OpenAlex, José M. Mateos has authored 18 papers receiving a total of 517 indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Endocrine and Autonomic Systems, 6 papers in Pediatrics, Perinatology and Child Health and 5 papers in Surgery. Recurrent topics in José M. Mateos's work include Circadian rhythm and melatonin (8 papers), Birth, Development, and Health (6 papers) and Parasite Biology and Host Interactions (4 papers). José M. Mateos is often cited by papers focused on Circadian rhythm and melatonin (8 papers), Birth, Development, and Health (6 papers) and Parasite Biology and Host Interactions (4 papers). José M. Mateos collaborates with scholars based in Spain, France and United States. José M. Mateos's co-authors include Miguel Fernández‐Bermejo, Lucía Ferrando‐Lamana, Cristina Ripoll, Nuria Fernández‐González, Javier Molina‐Infante, Moisés Hernández-Alonso, María González-Núñez, Carmen Dueñas, José Marı́a Pajares and Luis Fernández‐Salazar and has published in prestigious journals such as Scientific Reports, Clinical Cancer Research and International Journal of Molecular Sciences.

In The Last Decade

José M. Mateos

18 papers receiving 502 citations

Peers

José M. Mateos
Lea Paloheimo Finland
Pälvi Vento Finland
Y Geffroy France
Peter Friend United Kingdom
Nicola Leech United Kingdom
Khadija Hormi France
Davut Gül Türkiye
Antti‐Pekka Laine Finland
Antoine Soprani France
Takeki Hirano Japan
Lea Paloheimo Finland
José M. Mateos
Citations per year, relative to José M. Mateos José M. Mateos (= 1×) peers Lea Paloheimo

Countries citing papers authored by José M. Mateos

Since Specialization
Citations

This map shows the geographic impact of José M. Mateos's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by José M. Mateos with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites José M. Mateos more than expected).

Fields of papers citing papers by José M. Mateos

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by José M. Mateos. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by José M. Mateos. The network helps show where José M. Mateos may publish in the future.

Co-authorship network of co-authors of José M. Mateos

This figure shows the co-authorship network connecting the top 25 collaborators of José M. Mateos. A scholar is included among the top collaborators of José M. Mateos based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with José M. Mateos. José M. Mateos is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

18 of 18 papers shown
1.
Fernández‐Bermejo, Miguel, Gerardo Blanco‐Fernández, José M. Mateos, et al.. (2022). Melatonin controls cell proliferation and modulates mitochondrial physiology in pancreatic stellate cells. Journal of Physiology and Biochemistry. 79(1). 235–249. 8 indexed citations
2.
Fernández‐Bermejo, Miguel, José M. Mateos, Gerardo Blanco‐Fernández, et al.. (2021). Melatonin Induces Apoptosis and Modulates Cyclin Expression and MAPK Phosphorylation in Pancreatic Stellate Cells Subjected to Hypoxia. International Journal of Molecular Sciences. 22(11). 5555–5555. 12 indexed citations
3.
Martínez, Remigio, Alfredo García Sánchez, Mario Estévez, et al.. (2021). Melatonin Modulates the Antioxidant Defenses and the Expression of Proinflammatory Mediators in Pancreatic Stellate Cells Subjected to Hypoxia. Antioxidants. 10(4). 577–577. 9 indexed citations
4.
Gomes, Catarina, José M. Mateos, Rolando Pinho, et al.. (2020). The rebleeding rate in patients evaluated for obscure gastrointestinal bleeding after negative small bowel findings by device assisted enteroscopy. Revista Española de Enfermedades Digestivas. 112(4). 262–268. 6 indexed citations
5.
Peña, Fernando J., José A. Tapia, Miguel Fernández‐Bermejo, et al.. (2020). Melatonin modulates proliferation of pancreatic stellate cells through caspase-3 activation and changes in cyclin A and D expression. Journal of Physiology and Biochemistry. 76(2). 345–355. 13 indexed citations
6.
Fernández‐Bermejo, Miguel, et al.. (2020). The melatonin receptor antagonist luzindole induces the activation of cellular stress responses and decreases viability of rat pancreatic stellate cells. Journal of Applied Toxicology. 40(11). 1554–1565. 7 indexed citations
7.
González, Antonio, M. Salomé, Remigio Martínez, et al.. (2020). Melatonin modulates red-ox state and decreases viability of rat pancreatic stellate cells. Scientific Reports. 10(1). 21 indexed citations
8.
Salomé, M., Alfredo García Sánchez, Remigio Martínez, et al.. (2020). Pancreatic stellate cells exhibit adaptation to oxidative stress evoked by hypoxia. Biology of the Cell. 112(10). 280–299. 13 indexed citations
9.
Santofimia‐Castaño, Patricia, M. Salomé, Gerardo Blanco‐Fernández, et al.. (2019). Melatonin induces reactive oxygen species generation and changes in glutathione levels and reduces viability in human pancreatic stellate cells. Journal of Physiology and Biochemistry. 75(2). 185–197. 21 indexed citations
10.
Fernández‐Bermejo, Miguel, Gerardo Blanco‐Fernández, Diego López-Guerra, et al.. (2019). The melatonin receptor antagonist luzindole induces Ca2+ mobilization, reactive oxygen species generation and impairs trypsin secretion in mouse pancreatic acinar cells. Biochimica et Biophysica Acta (BBA) - General Subjects. 1863(11). 129407–129407. 8 indexed citations
11.
Tabernero, Josep, María Elena Elez, María Herranz‐López, et al.. (2014). A Pharmacodynamic/Pharmacokinetic Study of Ficlatuzumab in Patients with Advanced Solid Tumors and Liver Metastases. Clinical Cancer Research. 20(10). 2793–2804. 30 indexed citations
12.
Molina‐Infante, Javier, Lucía Ferrando‐Lamana, Cristina Ripoll, et al.. (2010). Esophageal Eosinophilic Infiltration Responds to Proton Pump Inhibition in Most Adults. Clinical Gastroenterology and Hepatology. 9(2). 110–117. 275 indexed citations
13.
14.
Rodero, M., Carmen Cuéllar, Soledad Fenoy, et al.. (2006). ELISA antibody determination in patients with anisakiosis or toxocariosis using affinity chromatography purified antigen. Allergy and Asthma Proceedings. 27(5). 422–428. 3 indexed citations
15.
16.
Perteguer, María Jesús, et al.. (2000). Specific and total IgE in patients with recurrent, acute urticaria caused by Anisakis simplex. Annals of Tropical Medicine and Parasitology. 94(3). 259–268. 4 indexed citations
17.
Gisbert, Javier P., Marı́a José Blanco, José M. Mateos, et al.. (1999). H. pylori-Negative Duodenal Ulcer Prevalence and Causes in 774 Patients. Digestive Diseases and Sciences. 44(11). 2295–2302. 73 indexed citations
18.
Olea, J.L., et al.. (1996). Frequency of congenital hypertrophy of the retinal pigment epithelium in familial adenomatous polyposis. Acta Ophthalmologica Scandinavica. 74(1). 48–50. 4 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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