The cardiovascular pathophysiology group is interested in the development of specific immunometabolic maps in the area of new therapeutic interventions in atherogenesis and cardiovascular diseases (CVD) leading to ischemia and/or heart failure. The correct adjustment of metabolism and homeostasis between the different cells that participate in the cardiovascular system are a key factor to ensure the correct and resolution of the inflammatory processes associated with CVD, including the introduction of therapeutic, dietary and lifestyle protocols. of life (microbiota). We are working as a mini-consortium providing a framework interested in:
- To assess the immunometabolic requirements to prevent plaque progression and to favor stability. Also, since some pathologies aggravate the atherogenic course (diabetes, cancer, etc.), this knowledge may provide evidence-based alternatives to avoid side effects on CVD.
- To improve therapeutic targeting to restrict remodeling of atheromatous macrophage
- To provide evidenced-based immunometabolic interventions to prevent macrophage recruitment and to ensure M2 pro-resolution activity.
- To determine the bioenergetic demands of macrophages under different polarization scenarios in the course of plaque dynamics.
- To generate metabolic and fluxomic maps that help to understand the complex regulatory networks operating inside the atheroma. At the same time, this comprehension of the metabolic fate may improve the non-invasive evaluation of the properties of the atheromatous plaque, by suppling substrates that increase the specificity and the tracer-to-background (TBR) in biomedical imaging (HF-NMR; PET/SPEC, etc.).
- To validate in human atheromatous cells the data issued from the rodent model of plaque formation, progression and stability, based under intervention of the mTOR and purinergic pathways, as well as the regulatory nodes that involve the correct activity of various nuclear receptors.
- To delve into the cellular and molecular events associated with adverse cardiac remodeling that appears in response to pathological stimuli such as aortic stenosis or myocardial infarction that will lead to heart failure over time. Provide information on new effective therapeutic targets in the prevention and/or reversal of this pathology
- Ensure the correct regulation of ion channels whose alteration generates various CVD pathologies.