Julio M. Martínez‐Moreno

University of Córdoba

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Juan R. Muñoz‐Castañeda

University of Córdoba

Mariano Rodríguez

Enel (Italy)

Yolanda Almadén

University of Córdoba

María E. Rodríguez‐Ortiz

Instituto Maimónides de Investigación Biomédica de Córdoba

Carmen Herencia

Hospital Universitario Fundación Jiménez Díaz

Escolástico Aguilera‐Tejero

University of Córdoba

Juan Miguel Díaz‐Tocados

Biomedical Research Institute of Lleida

Antonio Canalejo

Universidad de Huelva

Addy Montes de

Instituto Maimónides de Investigación Biomédica de Córdoba

Noemí Vergara

University of Córdoba

Cooperative Institutions

University of Córdoba

119

Instituto Maimónides de Investigación Biomédica de Córdoba

106

Hospital Universitario Reina Sofía

RELX Group (United States)

Instituto de Salud Carlos III

International Society of Nephrology

Institute for Research in Biomedicine

Universidad Autónoma de Madrid

Inserm

Hospital Universitario Fundación Jiménez Díaz

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Table of Contents

Kidney International (2019)

T. Alp İkizler Jai Radhakrishnan Germaine Wong Eric Siddall Sandro Mazzaferro

Table (database)

10.1016/s0085-2538(19)30348-5

Cite

Citations (0)

Calcium Deficiency Reduces Circulating Levels of FGF23

Journal of the American Society of Nephrology (2012)

María E. Rodríguez‐Ortiz José I. López Juan R. Muñoz‐Castañeda Julio M. Martínez‐Moreno Alan Peralta-Ramírez

Fibroblast growth factor (FGF) 23 inhibits calcitriol production, which could exacerbate calcium deficiency or hypocalcemia unless calcium itself modulates FGF23 in this setting. In Wistar rats with normal renal function fed a diet low in both calcium and vitamin D, the resulting hypocalcemia was associated with low FGF23 despite high parathyroid hormone (PTH) and high calcitriol levels. FGF23 correlated positively with calcium and negatively with PTH. Addition of high dietary phosphorus to this diet increased FGF23 except in rats with hypocalcemia despite high PTH levels. In parathyroidectomized rats, an increase in dietary calcium for 10 days increased serum calcium, with an associated increase in FGF23, decrease in calcitriol, and no change in phosphorus. Also in parathyroidectomized rats, FGF23 increased significantly 6 hours after administration of calcium gluconate. Taken together, these results suggest that hypocalcemia reduces the circulating concentrations of FGF23. This decrease in FGF23 could be a response to avoid a subsequent reduction in calcitriol, which could exacerbate hypocalcemia.

10.1681/asn.2011101006

Cite

Citations (201)

CKD BONE DISEASE

Nephrology Dialysis Transplantation (2014)

Juan Migueo Diaz-Tocados Carmen Herencia Julio M. Martínez‐Moreno A. Montes de María E. Rodríguez‐Ortiz

Bone disease

10.1093/ndt/gfu166

Cite

Citations (0)

Engineering parathyroid cells to treat secondary hyperparathyroidism

Kidney International (2009)

Mariano Rodríguez Julio M. Martínez‐Moreno Yolanda Almadén

Parathyroid chief cell

10.1038/ki.2008.635

Cite

Citations (2)

Ferroptosis and kidney disease

Nefrología (English Edition) (2020)

Diego Martín‐Sánchez Miguel Fontecha‐Barriuso Julio M. Martínez‐Moreno Adrián M. Ramos María Dolores Sánchez-Niño

Cell death is a finely regulated process occurring through different pathways. Regulated cell death, either through apoptosis or regulated necrosis offers the possibility of therapeutic intervention. Necroptosis and ferroptosis are among the best studied forms of regulated necrosis in the context of kidney disease. We now review the current evidence supporting a role for ferroptosis in kidney disease and the implications of this knowledge for the design of novel therapeutic strategies. Ferroptosis is defined functionally, as a cell modality characterized by peroxidation of certain lipids, constitutively suppressed by GPX4 and inhibited by iron chelators and lipophilic antioxidants. There is functional evidence of the involvement of ferroptosis in diverse forms of kidneys disease. In a well characterized nephrotoxic acute kidney injury model, ferroptosis caused an initial wave of death, triggering an inflammatory response that in turn promoted necroptotic cell death that perpetuated kidney dysfunction. This suggests that ferroptosis inhibitors may be explored as prophylactic agents in clinical nephrotoxicity or ischemia–reperfusion injury such as during kidney transplantation. Transplantation offers the unique opportunity of using anti-ferroptosis agent ex vivo, thus avoiding bioavailability and in vivo pharmacokinetics and pharmacodynamics issues. La muerte celular es un proceso minuciosamente regulado que se desarrolla a través de diferentes vías. La muerte celular regulada, ya sea mediante apoptosis o necrosis regulada, ofrece la posibilidad de introducir una intervención terapéutica. La necroptosis y la ferroptosis se encuentran entre las formas mejor estudiadas de necrosis regulada en el contexto de la nefropatía. Revisamos los datos actuales que avalan que la ferroptosis desempeña una función en la nefropatía y las repercusiones que tiene este conocimiento en el diseño de nuevas estrategias terapéuticas. La ferroptosis se define de forma funcional como una modalidad celular caracterizada por la peroxidación de ciertos lípidos, constitutivamente suprimida por GPX4 e inhibida por quelantes férricos y antioxidantes lipofílicos. Existen datos probatorios funcionales de la implicación de la ferroptosis en diversas formas de nefropatía. En un modelo de lesión renal aguda nefrotóxica bien caracterizado, la ferroptosis provocó una ola inicial de muerte, la cual desencadenó una respuesta inflamatoria que a su vez promovió la muerte celular necroptótica que perpetuó la disfunción renal. Esto sugiere que los inhibidores de la ferroptosis pueden explorarse como agentes profilácticos en la nefrotoxicidad clínica o en la lesión por isquemia-reperfusión, como durante un trasplante de riñón. Los trasplantes ofrecen una oportunidad única para el uso de agentes inhibidores de la ferroptosis ex vivo, con lo que se evitarían los problemas de biodisponibilidad y los problemas de farmacocinética y farmacodinámica in vivo.

Nephrotoxicity

Ex vivo

10.1016/j.nefroe.2020.09.006

Cite

Citations (20)

TGF-β Prevents Phosphate-Induced Osteogenesis through Inhibition of BMP and Wnt/β-Catenin Pathways

PLoS ONE (2014)

Fátima Guerrero Carmen Herencia Yolanda Almadén Julio M. Martínez‐Moreno Addy Montes de

Background Transforming growth factor-β (TGF-β) is a key cytokine during differentiation of mesenchymal stem cells (MSC) into vascular smooth muscle cells (VSMC). High phosphate induces a phenotypic transformation of vascular smooth muscle cells (VSMC) into osteogenic-like cells. This study was aimed to evaluate signaling pathways involved during VSMC differentiation of MSC in presence or not of high phosphate. Results Our results showed that TGF-β induced nuclear translocation of Smad3 as well as the expression of vascular smooth muscle markers, such as smooth muscle alpha actin, SM22α, myocardin, and smooth muscle-myosin heavy chain. The addition of high phosphate to MSC promoted nuclear translocation of Smad1/5/8 and the activation of canonical Wnt/β-catenin in addition to an increase in BMP-2 expression, calcium deposition and alkaline phosphatase activity. The administration of TGF-β to MSC treated with high phosphate abolished all these effects by inhibiting canonical Wnt, BMP and TGF-β pathways. A similar outcome was observed in high phosphate-treated cells after the inhibition of canonical Wnt signaling with Dkk-1. Conversely, addition of both Wnt/β-catenin activators CHIR98014 and lithium chloride enhanced the effect of high phosphate on BMP-2, calcium deposition and alkaline phosphatase activity. Conclusions Full VSMC differentiation induced by TGF-β may not be achieved when extracellular phosphate levels are high. Moreover, TGF-β prevents high phosphate-induced osteogenesis by decreasing the nuclear translocation of Smad 1/5/8 and avoiding the activation of Wnt/β-catenin pathway.

10.1371/journal.pone.0089179

Cite

Citations (52)

Exploring candidate biomarkers for rheumatoid arthritis through cardiovascular and cardiometabolic serum proteome profiling

Frontiers in Immunology (2024)

L. Cuesta-López Alejandro Escudero‐Contreras Y. Hanaee C. Pérez‐Sánchez M. Ruiz-Ponce

Introduction RA patients are at higher risk of cardiovascular disease, influenced by therapies. Studying their cardiovascular and cardiometabolic proteome can unveil biomarkers and insights into related biological pathways. Methods This study included two cohorts of RA patients: newly diagnosed individuals (n=25) and those with established RA (disease duration >25 years, n=25). Both cohorts were age and sex-matched with a control group (n=25). Additionally, a longitudinal investigation was conducted on a cohort of 25 RA patients treated with methotrexate and another cohort of 25 RA patients treated with tofacitinib for 6 months. Clinical and analytical variables were recorded, and serum profiling of 184 proteins was performed using the Olink technology platform. Results RA patients exhibited elevated levels of 75 proteins that might be associated with cardiovascular disease. In addition, 24 proteins were increased in RA patients with established disease. Twenty proteins were commonly altered in both cohorts of RA patients. Among these, elevated levels of CTSL1, SORT1, SAA4, TNFRSF10A, ST6GAL1 and CCL18 discriminated RA patients and HDs with high specificity and sensitivity. Methotrexate treatment significantly reduced the levels of 13 proteins, while tofacitinib therapy modulated the expression of 10 proteins. These reductions were associated with a decrease in DAS28. Baseline levels of SAA4 and high levels of BNP were associated to the non-response to methotrexate. Changes in IL6 levels were specifically linked to the response to methotrexate. Regarding tofacitinib, differences in baseline levels of LOX1 and CNDP1 were noted between non-responder and responder RA patients. In addition, response to tofacitinib correlated with changes in SAA4 and TIMD4 levels. Conclusion In summary, this study pinpoints molecular changes linked to cardiovascular disease in RA and proposes candidate protein biomarkers for distinguishing RA patients from healthy individuals. It also highlights how methotrexate and tofacitinib impact these proteins, with distinct alterations corresponding to each drug’s response, identifying potential candidates, as SAA4, for the response to these therapies.

Abatacept

10.3389/fimmu.2024.1333995

Cite

Citations (2)

Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration

Nephrology Dialysis Transplantation (2013)

María E. Rodríguez‐Ortiz Antonio Canalejo Carmen Herencia Julio M. Martínez‐Moreno Alan Peralta-Ramírez

The interest on magnesium (Mg) has grown since clinical studies have shown the efficacy of Mg-containing phosphate binders. However, some concern has arisen for the potential effect of increased serum Mg on parathyroid hormone (PTH) secretion. Our objective was to evaluate the direct effect of Mg in the regulation of the parathyroid function; specifically, PTH secretion and the expression of parathyroid cell receptors: CaR, the vitamin D receptor (VDR) and FGFR1/Klotho. The work was performed in vitro by incubating intact rat parathyroid glands in different calcium (Ca) and Mg concentrations. Increasing Mg concentrations from 0.5 to 2 mM produced a left shift of PTH–Ca curves. With Mg 5 mM, the secretory response was practically abolished. Mg was able to reduce PTH only if parathyroid glands were exposed to moderately low Ca concentrations; with normal–high Ca concentrations, the effect of Mg on PTH inhibition was minor or absent. After 6-h incubation at a Ca concentration of 1.0 mM, the expression of parathyroid CaR, VDR, FGFR1 and Klotho (at mRNA and protein levels) was increased with a Mg concentration of 2.0 when compared with 0.5 mM. Mg reduces PTH secretion mainly when a moderate low calcium concentration is present; Mg also modulates parathyroid glands function through upregulation of the key cellular receptors CaR, VDR and FGF23/Klotho system.

Parathyroid chief cell

Parathyroid gland

10.1093/ndt/gft400

Cite

Citations (135)

FP416PHOSPHATE RESTRICTION PRESERVES BONE VOLUME IN EARLY AND LATE STAGES OF CKD IN RATS

Nephrology Dialysis Transplantation (2015)

Juan Miguel Díaz‐Tocados María Encarnación Rodríguez Ortiz Carmen Herencia Julio M. Martínez‐Moreno Addy Montes de

10.1093/ndt/gfv177.15

Cite

Citations (0)

282 NUCLEAR TRANSLOCATION OF ß-CATENIN DURING MESENCHYMAL STEM CELLS DIFFERENTIATION INTO HEPATOCYTES IS ASSOCIATED WITH LIVER CANCER-RELATED PROTEINS

Journal of Hepatology (2012)

Carmen Herencia Julio M. Martínez‐Moreno Concha Herrera Fernando J. Corrales Isabel Espejo

10.1016/s0168-8278(12)60295-5

Cite

Citations (0)