Our research goal is to identify new strategies to targeting immune cells for boosting systemic resilience to inflammaging, cellular senescence and age-related multimorbidity.  Our most important discoveries in the last years are:

1. To demonstrate that mimicking age-associated mitochondrial dysfunction in T cells does not only recapitulate immunosenescence, but causes a general, body-wide deterioration of health with multiple aging-related features, including metabolic, musculoskeletal, cardiovascular and cognitive alterations, altogether resulting in premature death (Science, 2020). These results place the metabolism of T cells at the crossroad between inflammation, senescence and aging, highlighting that immunometabolism can be a therapeutic target to delay aging.
2. To decode the molecular mechanisms by which aged T cells contribute to inflammaging and age-related diseases. (a) Th1-Cytokines induce cellular senescence (b) Loss of Self-tolerance mechanisms. (c) Defective immuno-surveillance of senescent cells. (d) Altered gut microbiota. (Cell Metabolism 2021; Nature Rev Immunol, 2022; Annual Rev Immunol, in press).
3. To propose new therapeutic to reverse aortic aneurysms and prevent sudden death due to aortic dissections by boosting mitochondrial metabolism using NAD Precursors (Circulation, 2021; Atherosclerosis, Thrombosis Vascular Biology, 2022; Br J Pharmacol. 2022)