Notas Biográficas

Miguel P. Soares
Miguel Soares obtained his BS in biology (1990), MS in cellular biology (1994) and Ph.D. in Science (1995) at the University of Louvain, Belgium. He became a research fellow in the laboratory of Prof. Fritz H. Bach at the Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA (1995-1998), then instructor in surgery (1998- 2004) and lecturer (2003-2004) at Harvard Medical School, Boston, MA, USA. He moved to the “Instituto Gulbekian de Ciencia”, Oeiras, Portugal (2004) where he is currently a ”Principal Investigator”. He is also an invited professor at Lisbon Medical School, “Faculdade de Lisboa”, Portugal. The research developed by Miguel Soares laboratory at the “Instituto Gulbenkian de Ciência” evolves around understanding the cellular and molecular mechanisms regulating inflammation and how these can be used therapeutically to overcome the pathological outcome of immune mediated inflammatory diseases.

Main original scientific contributions include the finding that:
2012: Metabolic adaptation to tissue iron overload is essential to confer disease tolerance to systemic infections.
2011: Sickle hemoglobin confers disease tolerance to Plasmodium infection (Cell, 2011, Vol. 145, Issue 3, 398-409, 29).
2007-12: Heme oxygenase-1 supports the survival of an infected host irrespectively of pathogen load, providing a molecular basis for disease tolerance to Plasmodium (Nature Medicine, 2007, 13: 703-10 and Proc. Natl. Acad. Sci. USA. 2009, 106; 37: 15837-42) and polymicrobial (Science TM, 2010. 2: 51) infections (Science, 2012, 335, 936).
2007-10: The protective effects of the gaseous molecule carbon monoxide (CO) act via inhibition of heme release from hemoproteins, avoiding the deleterious effects of heme (Nature Medicine, 2007, 13:703-10 and Annu. Rev. Pharmacol. Toxicol. 2010. 50:323–54).
2001-7: The gaseous molecule CO can be used therapeutically to prevent the progression of a range of immune mediated inflammatory conditions, including the rejection of transplanted organs (J. Immunol, 2001, 166, 4185-4194, Nature Medicine, 2003, 9, 183-190), arteriosclerosis (Nature Medicine, 2003, 9, 183-190), ischemia & reperfusion injury (The FASEB Journal. 2004; 18:771-772), autoimmune neuroinflammation (J. Clin. Invest. 2007, 117, 438-447) or severe forms of malaria (Nature Medicine, 2007, 13: 703-10).
1998-2001: CO produced via heme catabolism by heme oxygenase-1, acts in a cytoprotective (J. Exp. Med., 2001, 192, 1015-25) and anti inflammatory (Nature Medicine, 2000, 6, 4, 422-428) manner.
1998: That transplanted organs express “protective genes”, i.e. heme oxygenase-1 that prevent graft rejection (Nature Medicine, 1998; 4, 91-8).

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