M
Mattia Albiero
Researcher at University of Padua
Publications - 89
Citations - 5779
Mattia Albiero is an academic researcher from University of Padua. The author has contributed to research in topics: Progenitor cell & Bone marrow. The author has an hindex of 35, co-authored 78 publications receiving 4807 citations.
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Journal ArticleDOI
Improved Function of Circulating Angiogenic Cells Is Evident in Type 1 Diabetic Islet-Transplanted Patients
Alessandra Petrelli,Anna Maestroni,Gian Paolo Fadini,Daniela Belloni,M. Venturini,Mattia Albiero,Sonja Kleffel,Bechara Mfarrej,A. Del Maschio,Paola Maffi,Angelo Avogaro,Elisabetta Ferrero,Gianpaolo Zerbini,Antonio Secchi,Paolo Fiorina +14 more
TL;DR: The data suggest that CAC function is altered in T1D and may be improved after islet transplantation, and in vivo an improved angiogenic ability of ITA compared to T2D was shown.
Journal ArticleDOI
Effects of SGLT2 Inhibitors on Circulating Stem and Progenitor Cells in Patients With Type 2 Diabetes.
TL;DR: In a cohort of 15 patients who received open-label empagliflozin for 12 weeks, CSCs declined nonsignificantly, whereas EPCs remained stable, thus, cardiovascular protection by SGLT2 inhibitors may not directly involve stem/progenitor cells.
Journal ArticleDOI
Rosuvastatin stimulates clonogenic potential and anti-inflammatory properties of endothelial progenitor cells.
Gian Paolo Fadini,Mattia Albiero,Elisa Boscaro,Lisa Menegazzo,Anna Cabrelle,Teodoro Piliego,Massimo Federici,Carlo Agostini,Angelo Avogaro +8 more
TL;DR: It is shown that rosuvastatin had significant stimulatory effects on EPCs irrespective of the culture protocol, and induced anti‐inflammatory polarization of monocytic E PCs.
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Restoring stem cell mobilization to promote vascular repair in diabetes.
TL;DR: Impaired stem cell mobilization in diabetes is described as a mechanism of failed vascular repair and evidence that pharmacological strategies can restore mobilization is provided and the pharmacological exploitation of the G-CSF/DPP-4(CD26)/SDF-1α axis is described.
Journal ArticleDOI
Myeloid calcifying cells promote atherosclerotic calcification via paracrine activity and allograft inflammatory factor-1 overexpression.
Mattia Albiero,Marcello Rattazzi,Lisa Menegazzo,Elisa Boscaro,Roberta Cappellari,Elisa Pagnin,Elisa Bertacco,Nicol Poncina,Kenneth A. Dyar,Stefano Ciciliot,Kazuya Iwabuchi,Renato Millioni,Giorgio Arrigoni,Nicolle Kraenkel,Ulf Landmesser,Carlo Agostini,Angelo Avogaro,Gian Paolo Fadini +17 more
TL;DR: It is shown that the murine spleen contains OC+BAP+ cells with a phenotype similar to human MCCs, a high expression of adhesion molecules and CD11b, and capacity to calcify in vitro and in vivo, which promote atherosclerotic calcification in ApoE−/− mice through paracrine activity and modulation of resident cells by AIF-1 overexpression.