Description

We are interested in what causes the accumulation of molecular damage that drives cellular aging and promotes the onset of diseases associated with aging such as cancer and neurodegeneration. Our goal is the mechanism of cellular adaptation over time that reshapes energy metabolism and the redox balance. Experimentally, we investigate the interaction between the bioenergetic and genomic remodeling that occurs throughout life, using biochemical assays and omic approaches on mouse models and human primary cells.

Current projects include the validation of mitochondrial dysfunctions related to aging in metastatic disease and the identification of epigenetic and metabolic signatures shared by aging and cognitive decline .

Five recent publications

1. Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity. Costantino S, Paneni F, Virdis A, Hussain S, Mohammed SA, Capretti G, Akhmedov A, Dalgaard K, Chiandotto S, Pospisilik JA, Jenuwein T, Giorgio M, Volpe M, Taddei S, Lüscher TF, Cosentino F. Eur Heart J. 2019. 40:383-91.

2. Epigenomic profiling of archived FFPE tissues by enhanced PAT-ChIP (EPAT-ChIP) technology. Amatori S, Persico G, Paolicelli C, Hillje R, Sahnane N, Corini F, Furlan D, Luzi L, Minucci S, Giorgio M, Pelicci PG, Fanelli M. Clin Epigenetics. 2018. 10:143.

3. Cyclophilin D counteracts P53-mediated growth arrest and promotes Ras tumorigenesis. Bigi A, Beltrami E, Trinei M, Stendardo M, Pelicci PG, Giorgio M. Oncogene. 2016. 35:5132-43.

4. P66SHC deletion improves fertility and progeric phenotype of late-generation TERC-deficient mice but not their short lifespan. Giorgio M, Stendardo M, Migliaccio E, Pelicci PG. Aging Cell. 2016. 15:446-54.

5. The mitochondrial translation machinery as a therapeutic target in Myc-driven lymphomas. A D.’Andrea, I Gritti, P Nicoli, M Giorgio, M Doni, A Conti, V Bianchi, LCasoli, A Sabò, A Mironov, GV Beznoussenko, B Amati. Oncotarget. 2016. 7:72415-30.