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Ana Belen Sanz
Researcher at Autonomous University of Madrid
Publications - 176
Citations - 8800
Ana Belen Sanz is an academic researcher from Autonomous University of Madrid. The author has contributed to research in topics: Kidney & Acute kidney injury. The author has an hindex of 47, co-authored 157 publications receiving 6673 citations. Previous affiliations of Ana Belen Sanz include Hospital Universitario La Paz & Complutense University of Madrid.
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Journal ArticleDOI
NF-κB in Renal Inflammation
Ana Belen Sanz,Maria Dolores Sanchez-Niño,Adrian M. Ramos,Juan Antonio Moreno,Beatriz Santamaría,Marta Ruiz-Ortega,Jesús Egido,Alberto Ortiz +7 more
TL;DR: Under most test conditions, specific NF-kappaB inhibitors tend to reduce inflammation in experimental kidney injury but not always, and although many drugs in current use clinically influence NF- kappaB activation, there are no data regarding specificNF-kappB inhibition in human kidney disease.
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Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury
Andreas Linkermann,Jan Hinrich Bräsen,Maurice Darding,Mi Kyung Jin,Ana Belen Sanz,Jan Ole Heller,Federica De Zen,Ricardo Weinlich,Alberto Ortiz,Henning Walczak,Joel M. Weinberg,Douglas R. Green,Ulrich Kunzendorf,Stefan Krautwald +13 more
TL;DR: It is demonstrated that necroptosis in ischemia–reperfusion injury (IRI) in mice occurs as primary organ damage, independent of the immune system, and that mice deficient for RIPK3, the essential downstream partner of RIPK1 in necroPTosis, are protected from IRI.
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The Inflammatory Cytokines TWEAK and TNFα Reduce Renal Klotho Expression through NFκB
Juan Antonio Moreno,María Concepción Izquierdo,Maria Dolores Sanchez-Niño,Beatriz Suarez-Alvarez,Carlos López-Larrea,Aniela Jakubowski,Julia Ramírez Blanco,Rafael J. Ramirez,Rafael Selgas,Marta Ruiz-Ortega,Jesús Egido,Alberto Ortiz,Ana Belen Sanz +12 more
TL;DR: Inflammatory cytokines, such as TWEAK and TNFα, downregulate Klotho expression through an NFκB-dependent mechanism, which may partially explain the relationship between inflammation and diseases characterized by accelerated aging of organs, including CKD.
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Ferroptosis, but Not Necroptosis, Is Important in Nephrotoxic Folic Acid–Induced AKI
Diego Martin-Sanchez,Olga Ruiz-Andres,Jonay Poveda,Susana Carrasco,Pablo Cannata-Ortiz,Maria Dolores Sanchez-Niño,Marta Ruiz Ortega,Jesús Egido,Andreas Linkermann,Alberto Ortiz,Ana Belen Sanz +10 more
TL;DR: It is shown that ferrostatin-1 (Fer-1), an inhibitor of ferroptosis, preserved renal function and decreased histologic injury, oxidative stress, and tubular cell death in this model, and that immunogenicity secondary to ferroPTosis may further worsen the damage, although necroptosis-related proteins may have additional roles in AKI.
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Tenofovir Nephrotoxicity: 2011 Update
Beatriz Fernandez-Fernandez,Ana Montoya-Ferrer,Ana Belen Sanz,Maria Dolores Sanchez-Niño,María Concepción Izquierdo,Jonay Poveda,Valeria Sainz-Prestel,Natalia Ortíz-Martín,Alejandro Parra-Rodríguez,Rafael Selgas,Marta Ruiz-Ortega,Jesús Egido,Alberto Ortiz +12 more
TL;DR: Despite initial cell culture and clinical trials results supporting the renal safety of tenofovir, its clinical use is associated with a low, albeit significant, risk of kidney injury, and regular monitoring of proximal tubular dysfunction and serum creatinine in high-risk patients is required to minimize nephrotoxicity.