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MARCO GIORGIO

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Position

Professore Associato

Address

VIA U. BASSI, 58/B - PADOVA

Telephone

+39 049 827 6060

Marco Giorgio obtained the bachelor's degree in biology after working on the transgenic model of HBV at the University of Rome in 1991. He completed the postgraduate training at IRBM in Pomezia, where he studied the biochemistry of IL-6. He was awarded a fellowship from AIRC to study gene function and develop cancer models at the Regina Elena Cancer Institute. Then, for another two years at the MSKCC in New York, he began to study the genetic link between cancer and aging. He obtained the doctorate in biotechnology discussing a thesis on the aging gene p66Shc and joined the IEO in Milan, where in the department of experimental oncology he has been studying the mechanisms of aging involved in tumorigenesis for two decades, and is currently investigating micrometastases.
Since 2018, he is associate professor of biochemistry at the department of biomedical science of the University of Padova, where he studies genomic reprogramming during aging.


Notices

Prof. Giorgio's lab on Web:

https://www.biomed.unipd.it/ricerca/aree-tematiche/mitochondrial-pathophysiology/aging-signaling-pathways/

https://www.research.ieo.it/research-and-technology/clinical-technoshots/clinical-technoshot-isolation-of-micrometastases-alive-cells/

https://www.instagram.com/aging_research_lab/

https://www.facebook.com/agingresearchlab/

Office hours

  • Friday from 10:00 to 12:00
    at Laboratorio del docente, Via Ugo Bassi 58/B, polo "Vallisneri" - piano 6 ala est - stanza 95

Publications

The results of Prof. Giorgio's research have been published in more than 150 publications on international journals in the fields of biochemistry, molecular biology, genetics, physiology, and medicine, listed in https://scholar.google.com/citations?user=qDBFcb0AAAAJ&hl=en, and cited about 15.000 times for an h-index of 52.

Last 2 years original publications:
1) Ketogenic diet and BHB rescue the fall of long-term potentiation in an Alzheimer's mouse model and stimulates synaptic plasticity pathway enzymes. Di Lucente et al. Commun Biol. 2024.7:195.
2) Caloric restriction leads to druggable LSD1-dependent cancer stem cells expansion. Pallavi et al. Nat Commun. 2024.15:828.
3) SIRT6 promotes metastasis and relapse in HER2-positive breast cancer. Andreani et al. Sci Rep. 2023.13:22000.
4) The early-life stress induced by oxytocin inhibition in p53 knockout mouse dams increases adulthood tumorigenesis in first and second generations. Stendardo et al. Cancer Reports. 2023.6:e1625.
5) Small molecule-induced epigenomic reprogramming of APL blasts leading to antiviral-like response and c-MYC downregulation. Amatori et al. Cancer Gene Ther. 2023.30:671-82.
6) Effect of the Enrichment in c-Kit Stem Cell Potential of Foetal Human Amniotic Fluid Cells: Characterization from Single Cell Analysis to the Secretome Content. Casciaro et al. Biomedicines. 2023.11:430.
7) Toll-like receptor 9 signaling after myocardial infarction: Role of P66SHCA adaptor protein. Baysa et al. Biochem Biophys Res Commun. 2023.644:70-8.
8) Time makes histone H3 modifications drift in mouse liver. Hillje et al. Aging. 2022 14:4959-75.
9) Hydroxycitric Acid Inhibits Chronic Myelogenous Leukemia Growth through Activation of AMPK and mTOR Pathway. Verrelli et al. Nutrients. 2022.14:2669.
10) Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells. Priami et al. Cell Death Differ. 2022.29:2429-44
11) Histone H3 lysine 4 and 27 trimethylation landscape of human alzheimer’s disease. Persico et al. Cells. 2022.11:734.
12) Dietary intake of cyanidin-3-glucoside induces a long-lasting cardioprotection from ischemia/reperfusion injury by altering the microbiota. Trinei et al. J Nutr Biochem. 2022.101:108921.
13) Hematopoietic progenitor cell liabilities and alarmins S100A8/A9-related inflammaging associate with frailty and predict poor cardiovascular outcomes in older adults. Bonora et al. Aging Cell. 2022.21:e13545.
14) Hematopoietic and non-hematopoietic p66Shc differentially regulates stem cell traffic and vascular response to ischemia in diabetes. Albiero et al. Antioxid Redox Signal. 2022.36:593-07.

Among the 5 most relevant:
1) Migliaccio et al. The p66shc adaptor protein controls oxidative stress response and life span in mammals. Nature.1999.402:309-13.
2) Giorgio et al. Electron transfer between cytochrome c and p66Shc generates reactive oxygen species that trigger mitochondrial apoptosis. Cell.2005.122:221-33.
3) Wang et al. Role of PML in cell growth and the retinoic acid pathway. Science.1998.279:1547-51.
4) Pinton et al. Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc. Science. 2007.315:659-63.
5) Butelli et al. Enrichment of tomato fruit with health-promoting anthocyanins by expression of select transcription factors. Nat Biotechnol. 2008.26:1301-8.

Research Area

Molecular mechanisms of aging, particularly physio-pathological mechanisms of genomic adaptation to the environment that shape energy and redox balance.

Genetic adaptation is assumed to be involved in aging and related organ dysfunction however it is largely unknown whether and how time reprograms cell identity and increases phenotypic heterogeneity. Our driving hypothesis is that cell-autonomous epigenetic errors, metabolic challenges and environmental stress responses lead to specific genomic remodeling that drive aging drifts. In collaboration with other research groups, we use in vitro systems, preclinical models, and samples from patients to study common histone codes and transcriptomic profiles of aging, associated cardiovascular diseases and neurodegeneration. By revealing the signature of genomic adaptation throughout life and by testing the rescue effect of epigenetic drugs and selected dietary interventions, we hope to identify biomarkers of disease risk and new treatments aimed at healthy aging.

- Ketogenic diet and BHB rescue the fall of long-term potentiation in an Alzheimer's mouse model and stimulates synaptic plasticity pathway enzymes. Di Lucente et al. Commun Biol. 2024.7:195.
- Histone H3 lysine 4 and 27 trimethylation landscape of human alzheimer’s disease. Persico et al. Cells. 2022.11:734.
- Time makes histone H3 modifications drift in mouse liver. Hillje et al. Aging. 2022.14:4959-75.

https://www.biomed.unipd.it/ricerca/aree-tematiche/mitochondrial-pathophysiology/aging-signaling-patways

Thesis proposals

Theses completed (last 5 years)
- Role and mechanisms of physical exercise in the prevention of colorectal cancer.
- Antileukemic effect of caloric restriction and of the plant bioactive hydroxycitric acid.
- The pathogenic mechanisms of steroid hormones used in sport.
- Supplementation of branched chain amino acids to increase muscle mass: risks and benefits.
- The relevance of the intake and origin of carbohydrates in the performance of a middle-distance athlete.
- The impact of the celiac diet on physical activity.
- Role of myocrobiota in the development of osteoarticular frailty in the elderly and effects of physical exercise.
- Bacteria in motion: the minimum amount of physical exercise necessary in order to improve the composition and functionality of the intestinal microbiota in obese and overweight subjects, avoiding the worsening of chronic low-grade inflammation.
- Role of alterations of the gut microbiota induced by physical exercise for the prevention of cardiovascular risk.
- The characteristics of the optimal physical activity program for patients with type 1 diabetes.
- Physical exercise and pre-diabetes: the best training strategies to combat this pathology.
- Neuroprotective role of myokines induced by resistance exercise in adults with mild cognitive impairment.
- The heart's response to pathogens: a genomic perspective via transcriptomic analysis.

Thesis topics available:
- Epigenetic effects of diets.
- Genomic reprogramming by protein aggregates and pollutants.
- On histone modifications during aging.