Eugénia Carvalho
+351 304502923
Principal Investigator
Group at CNC

Eugenia Carvalho is currently a principal investigator at the Center for Neuroscience and Cell Biology (CNC), University of Coimbra. She is the lider for the “Obesity, diabetes and complications” group. She did her undergraduate work in chemistry at Marymount Manhattan College in NYC, NY, USA.  Then she went to Sweden where she did her Masters and PhD in Molecular Medicine at the University of Gothenburg. Later as a research fellow she went to the Endocrinology Division  at Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School, Boston, US.
She has secured over a 1.3 million euros in funding and she has been the main supervisor of several Master and PhD students as well as Erasmus and post-doctoral students.



Area of Research: 

During her career she has focused her research in the context of chronic diseases in aging, such as insulin resistance, diabetes and its complications. Impaired wound healing is an important clinical problem in diabetes and results in failure to completely heal foot ulcers (DFU) seen in diabetes patients, eventually leading to lower extremity amputations. Her main interests have been to define systemic and local factors that are altered in diabetes and DFU and to identify dysfunctional signaling pathways in wound healing, essential for regeneration of skin tissue and enhancement of healing, with the goal of enhancing early diagnosis of patients at risk for chronic DFU and improving treatment, including new therapies and care of these patients. Several of her group’s main objectives have been to test several peptides that play important roles in skin regeneration and improved healing.

In addition, and for most of her career as a researcher she has been interested in understanding the role of the adipocyte as an endocrine and inflammatory organ. Adipocytes are important cells that regulate and cross-talk with most other important organs in the body key players in metabolism that are strongly affected by the aging body. One of the main efforts in her lab have been to try to understand the metabolic relationship between epicardial adipose tissue that surrounds the heart and the cardiomyocyte. More than any other organ adipose tissue is very plastic and can easily be modulated by physical activity and nutrition even as people age, and this is now one of the main focuses of her lab, the interaction between the adipocyte and skeletal muscle, in the aging population. In this context she has several active collaborations with scientists at both nationally as well as internationally.

Research Summary:
Selected Publications: 

1.    Leal EC, Carvalho E, Tellechea A, Kafanas A, Tecilazich F, Kearney C, Kuchibhotla S, Auster ME, Kokkotou E, Mooney DJ, LoGerfo FW, Pradhan-Nabzdyk L, Veves A. Substance P promotes wound healing in diabetes by modulating inflammation and macrophage phenotype. Am J Pathol. 2015 Jun;185(6):1638-48. IF 4.6
2.    Pereira M, Palming J, Rizell M, Aureliano M, Carvalho E, Svensson MK, Eriksson JW. Cyclosporine A and tacrolimus reduce the amount of GLUT4 at the cell-surface in human adipocytes: increased endocytosis as a potential mechanism for the diabetogenic effects of immunosuppressive agents. J Clin Endocrinol Metab. 2014 Oct;99(10):E1885-94. IF 6.4
3.    Moura LI, Dias A, Leal EC, Sousa H, Carvalho E. Chitosan-based dressings loaded with neurotensin – an efficient strategy to improve early diabetic wound healing. Acta Biomater. 2014 Feb;10(2):843-57. IF 5.68
4.    Lopes P, Fuhrmann A, Carvalho F, Sereno J, Santos M, Pereira MJ, Eriksson JW, Reis F, Carvalho E. Cyclosporine A enhances gluconeogenesis while Sirolimus impairs insulin signaling in peripheral tissues after 3 weeks of treatment. Biochem Pharmacol. 2014 Sep 1;91(1):61-73. IF 4.5
5.    Fuhrmann A, Lopes P, Sereno J, Pedro J, Espinoza D, Pereira MJ, Reis F, Eriksson JW, Carvalho E. Molecular mechanisms underlying the effects of cyclosporin A and sirolimus on glucose and lipid metabolism in liver, skeletal muscle and adipose tissue in an in vivo rat model. Biochem Pharmacol. 2014 Mar 15;88(2):216-28. IF 4.5


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Financiado por Fundos FEDER através do Programa Operacional Factores de Competitividade – COMPETE 2020 e por Fundos Nacionais através da FCT – Fundação para a Ciência e a Tecnologia no âmbito do projecto Estratégico com referência atribuida pelo COMPETE: POCI-01-0145-FEDER-007440

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