Antonio Musarò

Full Professor

antonio.musaro@uniroma1.it

Academic Appointments:

  • 1996−2000 Postdoctoral training− Research fellow, Cardiovascular Research Center; Harvard University.
  • 1999−2007 Assistant professor, Sapienza University of Rome −Medical School.
  • 2003−2014 Adjunct Associate Professor (honorary position), School of Biomedical & Sports Science; Faculty of Computing, Health and Science. Edith Cowan University; Western Australia.
  • 2007- Jan 2017 Associate professor, Medical and Biotechnology School, Sapienza University of Rome.
  • Feb 2017-present Full professor, Medical and Biotechnology School, Sapienza University of Rome
  • 2018-2024 Coordinator of the Ph.D. program in Morphogenesis and Tissue Engineering
  • 2020-present Senior Research Fellow and Coordinator of Life Science academic class, Sapienza School for Advanced Studies (SSAS)
  • 2024-present Director of Master in One Health, Sapienza University of Rome

Honors and Awards:

  • 2003 Award for Scientific Communication (Rotary Club)
  • 2006 Award for Scientific Communication, Foglia di Tabacco
  • 2009 Award Sapienza Ricerca for best research 2009 (Sapienza University of Rome)
  • 2014 La Plejade ANCIS International Award 2014 for Scientific Research
  • 2018 Unitel-Puglia (Pergamena D’onore)
  • 2021 Award “Union Invictus” for scientific career
  • 2024 Award «Alfredo Margreth» for Cell Biology, Accademia Nazionale dei Lincei

Scientific interests

Aging and neuromuscular diseases (ALS, muscular dystrophies); role of stem cells and tissue niche on muscle regeneration.

Contribution to Science

We study muscle homeostasis and regeneration under normal and pathologic conditions. Although considerable information has accumulated regarding the physiopathology of muscle diseases, the associated molecular mechanisms are still poorly understood. Current data point out that the development of muscle wasting is a multifactorial process and believed to be the result of both intrinsic factors, involving changes in molecular and cellular levels, and extrinsic ones, such as nutrition and exercise. We reported that motor-unit remodelling, decreased hormone levels with consequent negative effect on protein synthesis, stress oxidative damage, alteration in satellite cells activity may all contribute to decrease in muscle mass and functional performance.

Our approach entails both hypothesis-driven and data-driven investigations and combines an interdisciplinary set of expertise, ranging from cell, molecular, and biochemical tools, tissue engineering, material science and bio-mechanics approaches.

Selected publications

  • Musarò A, McCullagh KJ, Naya FJ, Olson EN, Rosenthal N. IGF-1 induces skeletal myocyte hypertrophy through calcineurin in association with GATA-2 and NF-ATc1. Nature. 1999; 400: 581-5.
  • Musarò A, McCullagh K, Paul A, Houghton L, Dobrowolny G, Molinaro M, Barton ER, Sweeney HL, Rosenthal N. Localized Igf-1 transgene expression sustains hypertrophy and regeneration in senescent skeletal muscle. Nature Genetics 2001; 27: 195-200.
  • Dobrowolny G, Giacinti C, Pelosi L, Nicoletti C, Winn N, Barberi L, Molinaro M, Rosenthal N, Musarò A. Muscle expression of a local Igf-1 isoform protects motor neurons in an ALS mouse model. J Cell Biol. 2005; 168:193-9.
  • Dobrowolny G, Aucello M, Rizzuto E, Beccafico S, Mammucari C, Bonconpagni S, Belia S, Wannenes, F Nicoletti, C Del Prete Z, Rosenthal N, Molinaro M, Protasi F, Fanò G, Sandri M, and Musarò A. Skeletal muscle is a primary target of SOD1G93A -mediated toxicity Cell Metabolism 2008; 8:425-36.
  • Cosentino M, Forcina L, Zouhair M, Apa L, Genovese D, Boccia C, Rizzuto E, Musarò A. Modelling three-dimensional cancer-associated cachexia and therapy: The molecular basis and therapeutic potential of interleukin-6 transignalling blockade. J Cachexia Sarcopenia Muscle. 2023;14(6):2550-2568. doi: 10.1002/jcsm.13329.

On-going Grants

Project Title ProjectFunding source Amount (Euros) Period Role of the PI
Dissecting mechanisms that cause cancer cachexia PRIN 85.500 2024-2026 PI
Are sympathetic neurons additional and targetable players in amyotrophic lateral sclerosis (ALS)? AriSLA 76.700 2023-2025 Co-PI
A translational approach to characterize the muscle-brain interplay in neurological non-communicable diseases. The M-Brain project Ministero della Salute 218.000 2024-2027 Co-PI

Complete list of published work in MyBibliography:
https://pubmed.ncbi.nlm.nih.gov/?term=musar%C3%B2+antonio&sort=date

KEYWORDS

Muscle homeostasis and regeneration, stem cells, neuromuscular diseases, aging, sarcopenia.

↑