Tissue homeostasis is the functional and structural maintenance of the organs of the body. It depends on as yet not fully understood genetic, molecular and cellular processes involved in the repair of structures and functions damaged by the normal functioning of the tissues or by environmental aggressions.
Stem cells residing in different organs of the adult are critical actors in the homeostasis process. Failures in this process provoke disease and cause aging.
Our program studies the genetic, molecular and cellular basis of the maintenance of the adult cardiovascular system. These studies are aimed at understanding the pathophysiological mechanisms involved in the origin and progression of lesions, and at the development of tissue engineering technologies for preserving or improving the regenerative capacity of cardiovascular tissues.
- Jose Antonio Enríquez Domínguez
- Program Coordinator
- Ext.2309
José Antonio Enríquez graduated in Biochemistry and Molecular Biology at the Universidad Autónoma de Madrid and obtained his PhD from the Universidad de Zaragoza in 1992. His thesis examined various aspects of mitochondrial DNA biogenesis.
From 1993 to 1997 he worked with G. Attardi at the California Institute of Technology, where he studied the pathogenic action of mutant mitochondrial tRNAs. His work in this period contributed to define the molecular mechanism underlying this phenomenon, and helped to establish the general methodologies for studying mitochondrial tRNAs. These methodologies have found application in studies of mitochondrial biogenesis and in the analysis of mtDNA-linked diseases. José Antonio established his own laboratory on his return to the Universidad de Zaragoza, where he became a Full Professor in 2007. His group has made important contributions to the understanding of mitochondrial biogenesis and bioenergetics, the role of mitochondria in apoptosis, the structure, formation and regulation of the respiratory chain, and the pathological consequences of altered mitochondrial function in human disease. He recently established a possible explanation for the phenotypes associated with common mouse mtDNA variants affecting ROS production. He joined the CNIC in 2009, where his work focuses on the molecular processes underlying the involvement of mitochondrial dysfunction in cardiovascular disease and ischemic processes.
© 2012 Centro Nacional de Investigaciones Cardiovasculares