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Javier Triñanes, PhD

I obtained my PhD in the University of La Laguna (Spain) supported by a fellowship from the Spanish Ministry of Education. During that period I studied inflammatory mechanisms in the vasculature of patients with end-stage chronic kidney disease. During my PhD we identified type-1 diabetic patients as the group with the worse vascular state at the moment of the kidney transplant (Diabetes Care. 2012 Feb;35(2):427-33). Specifically, we identified an important role for smooth muscle cells in the formation and progression of the atherosclerotic lesion in these patients, with important correlations between the vascular state and levels of IL-6, MCP-1 and VCAM-1 in the artery wall. Moreover, we also determined VCAM-1 as a potential marker of the progression of the disease after the transplant (PLoS One. 2015 Jun 12;10(6):e0129083). Since diabetes seemed to be one of the major causes for the development of additional complications, I got also very interested in their mechanisms. We described for the first time how the metabolic environment may be an essential factor for induction of beta-cell dysfunction by immunosuppressive therapies in animal models (Am J Transplant. 2013 Jul;13(7):1665-75).

In 2015, I obtained I travel grant from the European Foundation for the Study of Diabetes (EFSD) to come to the LUMC for learning how to work with primary cultures of human islets and I could join the islet research group thanks to a post-doctoral fellow funded by the Dutch Kidney Foundation.

Kidney and pancreas/islet transplantation are the best therapies for organ failure that we have nowadays. Immunosuppression in these patients is essential, but it may has some undesirable adverse effects. My research is focused in unveiling the molecular mechanisms by which immunosuppressive therapies affect negatively to beta-cells. Understanding these mechanism may lead us to better therapies to improve the outcomes and the function of the grafted tissue.

Find me on Researchgate or Linkedin.