Dr. Enriquez was born in Santiago de Compostela, SPAIN in 1963. He received the bachelor’s degree in Biochemistry and Molecular Biology in 1986 by the Universdidad Autonoma de Madrid (SPAIN) and the PhD degree in Science in 1992 by the Universidad de Zaragoza (SPAIN). His thesis was focused in the mtDNA biogenesis. From January 1993 to September 1997 he was post-doctoral scholar under the direction of Prof. Giuseppe Attardi at the California Institute of Technology in Pasadena, Ca (USA). There he studied the molecular mechanism of pathogenicity of mitochondrial tRNA mutations and contributed to stablish the general methodology to analyse mutant mitochondrial tRNAs. After finishing his post-doctoral stay in 1997 he moves to Zaragoza University first as Assistant Professor and initiate his own research group. In 1999 was promoted to Associated Professor and in 2006 to Full Professor both at Zaragoza University. In 1999 he moves his laboratory to the actual location at the National Centre for Cardiovascular Research in Madrid. There his work is focused on the implications of the natural genetic variability of OXPHOS genes in shaping metabolic differences between individuals, and the role of the dynamic modulation of the structure of the mitochondrial electron transport chain in health and disease. During 2006 he moves for a sabbatical leave to the MCR- MBU unit at Cambridge UK and from August 2014 to September 2015 he moves to Boston University at Boston, USA for another sabbatical leave.
Dr. Enriquez's research activity has focused on the study of mammalian mitochondrial electron transport chain (MtETC) and the ATP synthase, which constitute the oxidative phosphorylation system (OxPhos). For that, his group has developed strategies to determine the factors that regulate the structural organization of the electron transport chain. Thus, the work of Dr. Enriquez has shown that the established models of the organization of the electron transport chain were deficient, and that respiratory complexes could be organized into super structures or supercomplexes that coexist dynamically with the complexes in non-super assembled form. The work of Dr. Enriquez has explained the role that this super-structural organization plays in the metabolic adaptation, the production of reactive oxygen species (ROS), etc. He has also studied the role of ROS as mitochondrial second messengers and has begun to deconstruct the mammalian system OXPHOS in its functional components (electron transport, proton pumping and ATP synthesis) in cellular models. For more than 25 years, the research work led by Dr. José Antonio Enríquez has provided a scientific contribution in the following specific areas of several research lines. 1) Functional consequences of the genetic variability of the mtDNA, showing in human and mouse that the population variability of mtDNA conditions the metabolism of the organism, its response to drugs, predisposition to diseases, to healthy aging, etc. In addition, they demonstrate that certain mitochondrial variants may predispose to male infertility or are more frequent in tumors, and help explain the borderline pathology and functional variability for mtDNA alterations affecting tRNA mutations in patients. The same mutation they may cause the death of individuals of the same family while in others it does not caused any apparent symptoms despite being mutated 100% of the mtDNA of all individuals. 2) Development of new structural organization models of the electronic mitochondrial transport chain. the works of Dr. Enriquez group give rise to the proposal of the "Plasticity Model" to explain the dynamic organization of the mitochondrial electron transport chain, its regulation and its physiological significance. 3) The role of OxPhos in metabolic adaptation by which cells optimize and molecularly regulate their metabolic capacity, inducing structural changes in the electron transport chain and showed that the relevance of these adaptations in cardiovascular pathology, the immune system and in sensing hypoxia.
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