Our research focuses on studying the mitochondrial electron transport chain in mammals (MtETC) and the H⁺-ATP synthase, which constitute the oxidative phosphorylation system (OxPhos), as well as their implications for the regulation of organismal homeostasis, metabolism, and their physiopathological roles.

Our work aims to establish the interconnections between individual and population-level genomic structures encoding OxPhos function, their interaction with the environment (diet, lifestyle, exposome, etc.), and their causal involvement in rare diseases, common diseases (cardiovascular, neurological, metabolic), and healthy aging.

We integrate information about OxPhos function at various levels: biochemical, structural, genetic, cellular, tissue, organ, and whole organism. We perform comparative analyses across different vertebrates, such as zebrafish, mice, and humans. This approach enables us to study the functional consequences of genetic variability in mitochondrial DNA (mtDNA) and nuclear genes coding for OxPhos components. We also analyze how genetics shapes organismal metabolism, drug responses, disease predisposition, and healthy aging. Our goal is to explain the boundaries between pathology and functional variability in OxPhos system alterations. In particular, we examine the role of mitochondrial reactive oxygen species (ROS) as key signalers in the adaptation of the OxPhos system to the cell’s metabolic demands.

At the molecular level, we investigate the function of new structural organization models of mitochondrial electron transport, specifically our "Plasticity Model" to explain the dynamic organization of the mitochondrial respiratory chain. We explore the functional value of respiratory complex associations in superstructures and the connection between mitochondrial dynamics and bioenergetic function, aiming to understand how cells optimize and regulate their metabolic capacity molecularly by inducing structural changes in the electron transport chain.

We are particularly interested in the role of mitochondria in the development and homeostasis of the cardiovascular system, as well as their resilience and regenerative capacity in response to diseases. Thus, our goal is to understand the relevance of mitochondria and the OxPhos system in cardiac pathophysiology, including ischemia-reperfusion injury, heart failure, and cardiac electrical activity. Additionally, we investigate the mitochondrial role in inflammation, obesity, and vascular pathophysiology processes. Finally, we are interested in studying the contribution of mitochondrial genetics and its role as an integrative metabolic regulator in the process of healthy aging.