Raúl Rodrigues Díez

Profesor Ayudante Doctor

Universidad Complutense de Madrid

Spain

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Raúl Rodrigues Díez is an Assistant Professor at Universidad Complutense de Madrid, Spain. His research focuses on the molecular mechanisms underlying cardiac dysfunction, renal ischemia-reperfusion injury, and diabetic kidney disease, as evidenced by his recent publications. He investigates the role of cellular communication networks and epigenetic modifications in tissue response to stress and injury, aiming to develop targeted therapies for chronic conditions.

Articles (14)

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2024

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2024

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2024

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2024

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2022

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2022

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2022

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2022

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2022

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2022

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2022

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2022

Collaborators (9)

Vanesa Esteban

SPAIN

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Raquel Rodrigues Díez

Profesor ayudante doctor

Universidad Complutense de Madrid Facultad de Medicina

SPAIN

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Tri Q Nguyen

University Medical Center Groningen

NETHERLANDS

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José Tuñón

Head

Hospital Universitario Fundación Jiménez Díaz

SPAIN

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Jane Stubbe

aoosicate professor

University of Southern Denmark

DENMARK

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Andrew Leask

University of Saskatchewan

CANADA

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Martin Overgaard

Odense University Hospital

DENMARK

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Maria Jose GIMENO LONGAS

Assistant professor

Universidad Complutense de Madrid

SPAIN

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Marta Ruiz-Ortega

SPAIN

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Raúl Rodrigues Díez

Research Interests

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Articles (14)

Ccn2 Deletion Reduces Cardiac Dysfunction, Oxidative Markers, and Fibrosis Induced by Doxorubicin Administration in Mice

Smooth muscle-specific deletion of cellular communication network factor 2 causes severe aorta malformation and atherosclerosis

BET inhibitor nanotherapy halts kidney damage and reduces chronic kidney disease progression after ischemia-reperfusion injury

Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury

CCN2 (Cellular Communication Network Factor 2) Deletion Alters Vascular Integrity and Function Predisposing to Aneurysm Formation

The CCN2 Polymorphism rs12526196 Is a Risk Factor for Ascending Thoracic Aortic Aneurysm

Targeting inflammation to treat diabetic kidney disease: the road to 2030.

Cellular communication network 2 (connective tissue growth factor) aggravates acute DNA damage and subsequent DNA damage response-senescence-fibrosis following kidney ischemia reperfusion injury.

Demethylation of H3K9 and H3K27 Contributes to the Tubular Renal Damage Triggered by Endoplasmic Reticulum Stress

Editorial: Mechanisms Underlying Diabetes-Associated Damage in Target Tissues

Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice

CCN2 Binds to Tubular Epithelial Cells in the Kidney

Oxidative Stress and Cellular Senescence Are Involved in the Aging Kidney

Epigenetic Modulation of Gremlin-1/NOTCH Pathway in Experimental Crescentic Immune-Mediated Glomerulonephritis

Collaborators (9)

Vanesa Esteban

Raquel Rodrigues Díez

Tri Q Nguyen

José Tuñón

Jane Stubbe

Andrew Leask

Martin Overgaard

Maria Jose GIMENO LONGAS

Marta Ruiz-Ortega

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