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23 results on '"Raglianti, Valentina"'

3. A Clinical Workflow for Cost-Saving High-Rate Diagnosis of Genetic Kidney Diseases

Author

Becherucci, Francesca, Landini, Samuela, Palazzo, Viviana, Cirillo, Luigi, Raglianti, Valentina, Lugli, Gianmarco, Tiberi, Lucia, Dirupo, Elia, Bellelli, Stefania, Mazzierli, Tommaso, Lomi, Jacopo, Ravaglia, Fiammetta, Sansavini, Giulia, Allinovi, Marco, Giannese, Domenico, Somma, Chiara, Spatoliatore, Giuseppe, Vergani, Debora, Artuso, Rosangela, Rosati, Alberto, Cirami, Calogero, Dattolo, Pietro Claudio, Campolo, Gesualdo, De Chiara, Letizia, Papi, Laura, Vaglio, Augusto, Lazzeri, Elena, Anders, Hans-Joachim, Mazzinghi, Benedetta, and Romagnani, Paola

Published
2023
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4. Polyploid tubular cells initiate a TGF-β1 controlled loop that sustains polyploidization and fibrosis after acute kidney injury

Author

De Chiara, Letizia, primary, Semeraro, Roberto, additional, Mazzinghi, Benedetta, additional, Landini, Samuela, additional, Molli, Alice, additional, Antonelli, Giulia, additional, Angelotti, Maria Lucia, additional, Melica, Maria Elena, additional, Maggi, Laura, additional, Conte, Carolina, additional, Peired, Anna Julie, additional, Cirillo, Luigi, additional, Raglianti, Valentina, additional, Magi, Alberto, additional, Annunziato, Francesco, additional, Romagnani, Paola, additional, and Lazzeri, Elena, additional

Published
2023
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7. Differentiation of crescent-forming kidney progenitor cells into podocytes attenuates severe glomerulonephritis in mice

Author

Melica, Maria Elena, primary, Antonelli, Giulia, additional, Semeraro, Roberto, additional, Angelotti, Maria Lucia, additional, Lugli, Gianmarco, additional, Landini, Samuela, additional, Ravaglia, Fiammetta, additional, Regina, Gilda La, additional, Conte, Carolina, additional, De Chiara, Letizia, additional, Peired, Anna Julie, additional, Mazzinghi, Benedetta, additional, Donati, Marta, additional, Molli, Alice, additional, Steiger, Stefanie, additional, Magi, Alberto, additional, Bartalucci, Niccolò, additional, Raglianti, Valentina, additional, Guzzi, Francesco, additional, Maggi, Laura, additional, Annunziato, Francesco, additional, Burger, Alexa, additional, Lazzeri, Elena, additional, Anders, Hans-Joachim, additional, Lasagni, Laura, additional, and Romagnani, Paola, additional

Published
2022
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8. Clinical and Genetic Characterization of Patients with Bartter and Gitelman Syndrome

Author

Palazzo, Viviana, primary, Raglianti, Valentina, additional, Landini, Samuela, additional, Cirillo, Luigi, additional, Errichiello, Carmela, additional, Buti, Elisa, additional, Artuso, Rosangela, additional, Tiberi, Lucia, additional, Vergani, Debora, additional, Dirupo, Elia, additional, Romagnani, Paola, additional, Mazzinghi, Benedetta, additional, and Becherucci, Francesca, additional

Published
2022
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10. FC036: A Clinical Workflow for Selection of Patients and Cost-Efficient Diagnosis of Genetic Kidney Diseases

Author

Becherucci, Francesca, primary, Cirillo, Luigi, additional, Landini, Samuela, additional, Palazzo, Viviana, additional, Raglianti, Valentina, additional, Lugli, Gianmarco, additional, Tiberi, Lucia, additional, Vaglio, Augusto, additional, Anders, Hans-Joachim, additional, Mazzinghi, Benedetta, additional, and Romagnani, Paola, additional

Published
2022
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11. MO1057: Cost-Analysis of a Clinical Workflow for Diagnosis of Inherited Kidney Diseases

Author

Cirillo, Luigi, primary, Becherucci, Francesca, additional, Bellelli, Stefania, additional, Mazzinghi, Benedetta, additional, Raglianti, Valentina, additional, Lugli, Gianmarco, additional, Landini, Samuela, additional, Palazzo, Viviana, additional, Tiberi, Lucia, additional, Vaglio, Augusto, additional, Anders, Hans-Joachim, additional, and Romagnani, Paola, additional

Published
2022
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17. Cheyne-Stokes respiration related oscillations in cardiopulmonary hemodynamics in patients with heart failure

Author

Giannoni, Alberto, primary, Raglianti, Valentina, additional, Taddei, Claudia, additional, Borrelli, Chiara, additional, Chubuchny, Vladislav, additional, Vergaro, Giuseppe, additional, Mirizzi, Gianluca, additional, Valleggi, Alessandro, additional, Cameli, Matteo, additional, Pasanisi, Emilio, additional, Emdin, Michele, additional, and Passino, Claudio, additional

Published
2019
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18. Idiopathic retroperitoneal fibrosis: an update for nephrologists.

Author

Raglianti, Valentina, Rossi, Giovanni M., and Vaglio, Augusto

Subjects
*RETROPERITONEAL fibrosis, *AUTOIMMUNITY, *ADRENOCORTICAL hormones, *HYDRONEPHROSIS, *RITUXIMAB
Abstract

Idiopathic retroperitoneal fibrosis (IRF) is a rare condition characterized by the development of a peri-aortic and peri-iliac tissue showing chronic inflammatory infiltrates and pronounced fibrosis. Ureteral entrapment with consequent obstructive uropathy is one of the most common complications of IRF, which can lead to acute renal failure and, in the long term, to varying degrees of chronic kidney disease. IRF may be isolated or develop in association with autoimmune diseases (e.g. Hashimoto's thyroiditis and psoriasis) and other fibro-inflammatory disorders (often within the spectrum of immunoglobulin G4-related disease), which suggests that it should be considered as a potentially systemic condition. IRF is an immune-mediated disease: genetic variants (e.g. human leukocyte antigen (HLA)-DRB1*03) and environmental agents (mainly exposure to asbestos and smoking) are strongly associated with an increased risk of developing the disease, while a complex network of chemokines (e.g. CXCL12 and C-C moti chemokine 11 (CCL11)) and cytokines [e.g. interleukin (IL)-6, IL-12 and IL-13] is likely to orchestrate the inflammatory response and simultaneously promote fibrosis. Glucocorticoids, alone or in combination with traditional immunosuppressants such as methotrexate and mycophenolate mofetil, are usually efficacious and promptly induce disease remission; however, up to 50% of patients relapse, thus requiring repeat immunosuppressive courses. Biologic drugs, namely rituximab, are being explored for the treatment of IRF. In addition to medical therapies, interventional procedures (mainly ureteral stenting) are required to relieve ureteral obstruction, whereas surgical ureterolysis is generally reserved to refractory cases. If appropriately treated, then the overall and renal prognosis of IRF are good, with <5% patients developing end-stage renal disease. [ABSTRACT FROM AUTHOR]

Published
2021
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20. Targeting Mitochondrial Dysfunction in Chronic Heart Failure: Current Evidence and Potential Approaches

Author

Aimo, Alberto, primary, Borrelli, Chiara, additional, Vergaro, Giuseppe, additional, F. Piepoli, Massimo, additional, R. De Caterina, Alberto, additional, Mirizzi, Gianluca, additional, Valleggi, Alessandro, additional, Raglianti, Valentina, additional, Passino, Claudio, additional, Emdin, Michele, additional, and Giannoni, Alberto, additional

Published
2016
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21. Abstract 18963: Clinical Significance of Daytime Vs. Nighttime Cheyne-stokes Respiration in Systolic Heart Failure Patients: Findings From 24- Hour Polygraphic Recordings

Author

Mirizzi, Gianluca, primary, Iudice, Giovanni, additional, Bramanti, Francesca, additional, Giannoni, Alberto, additional, Poletti, Roberta, additional, Gabutti, Alessandra, additional, Mammini, Chiara, additional, Raglianti, Valentina, additional, Passino, Claudio, additional, and Emdin, Michele, additional

Published
2014
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23. Polyploid tubular cells initiate a TGF-β1 controlled loop that sustains polyploidization and fibrosis after acute kidney injury.

Author

De Chiara L, Semeraro R, Mazzinghi B, Landini S, Molli A, Antonelli G, Angelotti ML, Melica ME, Maggi L, Conte C, Peired AJ, Cirillo L, Raglianti V, Magi A, Annunziato F, Romagnani P, and Lazzeri E

Subjects
Animals, Mice, Epithelial Cells, Polyploidy, Fibrosis, Transforming Growth Factor beta1 genetics, Acute Kidney Injury genetics
Abstract

Polyploidization of tubular cells (TC) is triggered by acute kidney injury (AKI) to allow survival in the early phase after AKI, but in the long run promotes fibrosis and AKI-chronic kidney disease (CKD) transition. The molecular mechanism governing the link between polyploid TC and kidney fibrosis remains to be clarified. In this study, we demonstrate that immediately after AKI, expression of cell cycle markers mostly identifies a population of DNA-damaged polyploid TC. Using transgenic mouse models and single-cell RNA sequencing we show that, unlike diploid TC, polyploid TC accumulate DNA damage and survive, eventually resting in the G1 phase of the cell cycle. In vivo and in vitro single-cell RNA sequencing along with sorting of polyploid TC shows that these cells acquire a profibrotic phenotype culminating in transforming growth factor (TGF)-β1 expression and that TGF-β1 directly promotes polyploidization. This demonstrates that TC polyploidization is a self-sustained mechanism. Interactome analysis by single-cell RNA sequencing revealed that TGF-β1 signaling fosters a reciprocal activation loop among polyploid TC, macrophages, and fibroblasts to sustain kidney fibrosis and promote CKD progression. Collectively, this study contributes to the ongoing revision of the paradigm of kidney tubule response to AKI, supporting the existence of a tubulointerstitial cross talk mediated by TGF-β1 signaling produced by polyploid TC following DNA damage. NEW & NOTEWORTHY Polyploidization in tubular epithelial cells has been neglected until recently. Here, we showed that polyploidization is a self-sustained mechanism that plays an important role during chronic kidney disease development, proving the existence of a cross talk between infiltrating cells and polyploid tubular cells. This study contributes to the ongoing revision of kidney adaptation to injury, posing polyploid tubular cells at the center of the process.

Published
2023
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