Our research
Our research
Historically, mitochondria have been only considered the centers of energy production in the cell. However, besides driving respiration and ATP production, mitochondria are central regulators of many other cellular functions, which include cell death, cell differentiation, signaling, and anabolism, among others. In keeping with this, alterations in mitochondrial biology are bound to have a major impact on disease. Mitochondrial alterations and dysfunction have been implicated in inherited mitochondrial diseases, neurodegenerative and metabolic diseases such as type 2 diabetes (T2D) and vascular disease, aging, and cancer. Hence, mitochondria have emerged as powerful pharmacological targets in the treatment of many human diseases.
Mitochondria can also be considered integrator hubs connecting different cellular signals to the generation of an appropriate response to maintain cell homeostasis. However, although many advances have been done in the last years in the understanding of the involvement of mitochondria in different cellular processes, less is known about the molecular mechanisms involved in the integration of external cues and signals and generation of mitochondrial responses (mitochondrial signaling). The goal of our research is to study and identify molecular pathways involved in mitochondrial signaling, quality, and function, and its involvement in the development of complex diseases, with special emphasis on metabolic diseases and age-related pathologies. These studies will contribute to a broader understanding of how mitochondrial dysfunction is connected to disease and will potentially provide the rationale to target mitochondrial fitness to develop new therapeutic and pharmacological approaches to treat age-related diseases. Specifically, using both in vitro cell cultured models and in vivo genetically modified mice, our research is focused on whether alterations in mitochondrial signaling and quality are a key event in the loss of cell and tissue homeostasis and the development of disease.
Mitochondria are essential organelles that require continuous surveillance mechanisms to maintain their functional integrity. In this regard, mitophagy and mitochondrial dynamics serve as major quality control mechanisms to preserve mitochondrial fitness. Our laboratory is interested in the study of mitochondrial signaling pathways that could have a role in maintenance of mitochondrial health and their connection with metabolic disease and age-related pathologies, such as age-related sarcopenia.
Metabolic adaptation to external cues is a key process in the maintenance of cellular homeostasis. Although mitochondria play an essential role in metabolism, their precise role in the metabolic adaptation has only started to be elucidated. We aim to elucidate mitochondrial signaling pathways which could be inovolved in the regulation of metabolic adapation to different physiological and pathological contexts, and their role in disease.
Mitochondrial dysfunction is a hallmark of several age-related diseases. By using high-throughput and phenotypic screenings, our laboratory is interested in the finding of new small molecules promoting mitochondrial function and fitness for the treatment of metabolic diseases and/or other diseases characterized by mitochondrial alterations.