Gian Paolo Fadini

Prof. Dr. Gian Paolo Fadini

1. Department of Medicine, University of Padova, Padua, Italy</br>2. Venetian Institute of Molecular Medicine, Padova, Italy
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Research Focus & Metrics

Academic Career Length

24Years (2003-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2005 in JACC
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Journal Article
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Gian Paolo FadiniGian Paolo Fadini
Gian Paolo Fadini
MMMarta Miorin
Marta Miorin
MFMonica Facco
Monica Facco
SBSondra Bonamico
Sondra Bonamico
IBIlenia Baesso
Ilenia Baesso
AAAngelo Avogaro
Angelo Avogaro

17 February 2012 in Circulation Research
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Journal Article
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Gian Paolo FadiniGian Paolo Fadini
Gian Paolo Fadini
DLDouglas Losordo
Douglas Losordo
DBDittmar Böckler
Dittmar Böckler
Diverse subsets of endothelial progenitor cells (EPCs) are used for the treatment of ischemic diseases in clinical trials, and circulating EPCs levels are considered as biomarkers for coronary and peripheral artery disease. However, despite significant steps forward in defining their potential for both therapeutic and diagnostic purposes, further progress has been mired by unresolved questions around the definition and the mechanism of action of EPCs. Diverse culturing methods and detection of various combinations of different surface antigens were used to enrich and identify EPCs. These attempts were particularly challenged by the close relationship and overlapping markers of the endothelial and hematopoietic lineages. This article will critically review the most commonly used protocols to define EPCs by culture assays or by fluorescence-activated cell sorter in the context of their therapeutic or diagnostic use. We also delineate new research avenues to move forward our knowledge on EPC biology.

31 July 2023 in Cardiovascular Diabetology
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MMMarella Marassi
Marella Marassi
Gian Paolo FadiniGian Paolo Fadini
Gian Paolo Fadini
Type 2 diabetes (T2D), cardiovascular disease (CVD) and chronic kidney disease (CKD), are recognized among the most disruptive public health issues of the current century. A large body of evidence from epidemiological and clinical research supports the existence of a strong interconnection between these conditions, such that the unifying term cardio-metabolic-renal (CMR) disease has been defined. This coexistence has remarkable epidemiological, pathophysiologic, and prognostic implications. The mechanisms of hyperglycemia-induced damage to the cardio-renal system are well validated, as are those that tie cardiac and renal disease together. Yet, it remains controversial how and to what extent CVD and CKD can promote metabolic dysregulation. The aim of this review is to recapitulate the epidemiology of the CMR connections; to discuss the well-established, as well as the putative and emerging mechanisms implicated in the interplay among these three entities; and to provide a pathophysiological background for an integrated therapeutic intervention aiming at interrupting this vicious crosstalks.

28 March 2020 in Journal of Endocrinological Investigation
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Gian Paolo FadiniGian Paolo Fadini
Gian Paolo Fadini
MMM. L. Morieri
M. L. Morieri
ELE. Longato
E. Longato
AAA. Avogaro
A. Avogaro

22 April 2011 in Diabetes Care
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Journal Article
Open access
AAAngelo Avogaro
Angelo Avogaro
MAMattia Albiero
Mattia Albiero
LMLisa Menegazzo
Lisa Menegazzo
SKSaula de Kreutzenberg
Saula de Kreutzenberg
Gian Paolo FadiniGian Paolo Fadini
Gian Paolo Fadini

1 September 2006 in Arteriosclerosis, Thrombosis, and Vascular Biology
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Journal Article
Closed access
Gian Paolo FadiniGian Paolo Fadini
Gian Paolo Fadini
SSSaverio Sartore
Saverio Sartore
MAMattia Albiero
Mattia Albiero
IBIlenia Baesso
Ilenia Baesso
EMEllen Murphy
Ellen Murphy
AAAngelo Avogaro
Angelo Avogaro
Objective— Peripheral arterial disease (PAD) is a threatening complication of diabetes. As endothelial progenitor cells (EPCs) are involved in neovasculogenesis and maintenance of vascular homeostasis, their impairment may have a role in the pathogenesis of diabetic vasculopathy. This study aimed to establish whether number and function of EPCs correlate with PAD severity in type 2 diabetic patients. Methods and Results— EPCs were defined by the expression of CD34, CD133 and KDR, and quantified by flow cytometry in 127 diabetic patients with and without PAD. PAD severity has been assessed as carotid atherosclerosis and clinical stage of leg atherosclerosis obliterans. Diabetic patients with PAD displayed a significant 53% reduction in circulating EPCs versus non-PAD patients, and EPC levels were negatively correlated with the degree of carotid stenosis and the stage of leg claudication. Moreover, the clonogenic and adhesion capacity of cultured EPCs were significantly lower in diabetic patients with PAD versus patients without. Conclusions— This study demonstrates that EPC decrease is related to PAD severity and that EPC function is altered in diabetic subjects with PAD, strengthening the pathogenetic role of EPC dysregulation in diabetic vasculopathy. EPC count may be considered a novel biological marker of peripheral atherosclerosis in diabetes.