BIO

Education and Training

1996: M.Sc. Pharmaceutical Chemistry and Technology, Università degli Studi, Milan, Italy.

2000: PhD Biotechnology, Università degli Studi, Milan, Italy.

2005: Ms. in Science Communication, Università di Ferrara, Ferrara, Italy.

2000-2005: Postdoctoral Training, San Raffaele scientific Institute, Milan, Italy.

2010-2011 (short stages): Visiting Professor, Department of Pathology, School of Medicine, University of Utah, Salt Lake City, UT, USA.

Positions and Employment

2007-present: Adjunct Professor of “Tecniche Sperimentali Molecolari” and Tutor within the course of Medical Genetics, Vita-Salute University, Milan, Italy.

2005-2015: Research Associate, Regulation of Iron Metabolism Unit, OSR, Milan, Italy.

2016: Project leader, OSR, Milan, Italy.

Membership and appointments

2015-2019: Member of the Board of Directors, International BioIron Society (IBIS)

2018-2020: Member of the Scientific Program Committee-Advisory Board “Red cells and iron”, European Hematology Association (EHA)

2019-2021: Member of the Scientific Committee on Iron and Heme, American Society of Hematology (ASH)

2021-2023: Vice-Chair and Chair of the Scientific Committee on Iron and Heme, ASH

2023-present: Member of EHA-Scientific Working Group on Red Cell and Iron metabolism

Honors

2009: XV Telethon Convention. Best poster award.

2013: IBIS, London, UK. Gunshin-Levy award.

Financial support

Telethon Foundation, Cariplo Telethon Alliance, the Italian Ministry of Health, PRIN.

LAB

Brief Introduction

The BMP-SMAD signaling pathway plays a crucial role in several fundamental biological processes, including iron metabolism. In the liver, this signaling pathway is responsible for the regulation of hepcidin expression, the key hormone regulating iron homeostasis. Defective regulation of the BMP-SMAD pathway leads to iron-related diseases such as hereditary hemochromatosis, characterized by inhibition of the BMP-SMAD pathway and iron overload due to decreased hepcidin production, or Iron Refractory Iron Deficiency Anemia (IRIDA), in which constitutive activation of the BMP-SMAD pathway leads to iron deficiency anemia due to increased hepcidin synthesis. Despite recent progress in understanding the mechanisms regulating the BMP-SMAD signaling pathway in the liver, it is still not fully understood how this pathway is controlled. Furthermore, little is known about how this signaling pathway modulates biochemical processes in the liver under physiological and pathological conditions.

Research activity

Our research activities are mainly focused on iron- and metabolic-related diseases, with an emphasis on metabolic dysfunction-associated fatty liver disease (MASLD), one of the most common chronic liver diseases in industrialized countries, which is characterized by steatosis with liver inflammation and can lead to metabolic dysfunction-associated steatohepatitis (MASH), advanced fibrosis, cirrhosis and hepatocellular carcinoma. Several lines of evidence (literature data and our preliminary data) suggest that the hepatic BMP-SMAD pathway (and iron metabolism) may shape the metabolic profile of the liver and influence disease development.

Our research interests are mainly focused on:

1. Deciphering the mechanisms of hepcidin and BMP-SMAD pathway regulation in physiologic and pathologic conditions associated with deregulated iron metabolism, such as hereditary hemochromatosis, iron refractory iron deficiency anemia (IRIDA) and beta-thalassemia.

2. Investigating the role of the hepatic BMP-SMAD signaling pathway in the development of MASLD-MASH and the potential beneficial effect of its pharmacological manipulation.

3. To understand the contribution of two methyltransferases, Suv420h1 and Suv420h2, potentially involved in the crosstalk between iron-BMP-SMAD signaling pathway and lipid metabolism, to the development of MASLD-MASH and their pharmacological manipulation to counteract disease progression.

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