Cardiovascular diseases (CVD) represent the main cause of death and their high prevalence implies a high health cost, in addition to increasing physical dependence and reducing the quality of aging of the population. Therefore, understanding the molecular basis of CVD is a priority to mitigate the high number of deaths and current chronic patients. Likewise, knowledge of the mechanisms involved in correct cardiac formation and function could contribute to developing health prevention strategies.
The canonical response to hypoxia provides a ubiquitous mechanism of adaptation to low oxygen supply. The variety of processes regulated by hypoxia include metabolic reprogramming, vascularization, immune response modulation, pluripotency, differentiation and survival or migration, among many others. Therefore, the pathophysiology of hypoxia is broad and complex, and it is a clinical priority to unravel the molecular mechanisms that link HIF-mediated signaling with highly prevalent human diseases, such as metabolic disorders or CVD.
Oxygen is an essential modulator of the cardiovascular system and is involved in the appearance and evolution of numerous CVD. The general objective of our group is focused on understanding how hypoxia signaling impacts cardiovascular development and homeostasis and on defining the molecular mechanisms that orchestrate adaptation to changes in oxygen levels in both physiological and pathological conditions.
Our main lines of work include:
1. To determine the role of the VHL/HIF axis in the development and maturation of the heart
2. Identifying the molecular mechanisms connecting hypoxia signaling with prevalent CV diseases such as cardiac hypertrophy and pulmonary hypertension
3. The characterization of the cellular and molecular events controlled by HIF transcription factors and VHL in coronary homeostasis and vascular pathologies
4. To understand the importance of hypoxia-mediated signaling in cardiac regeneration