Hutchinson-Gilford progeria syndrome (HGPS) is a rare condition characterized by premature aging, furthermore the main caused of demise is hearth failure. HGPS is caused by the presence of progerin, the aberrant protein derived from LMNA/C gene mutation. On the other hand, D-β-hydroxybutyrate, BHB, has been previously proposed as an anti-senescent agent in vitro and in vivo. Moreover, the use of BHB derivatives as ketone esters slows the heart decline in mice with heart failure. Here, we provide evidence of BHB therapeutic effect on HGPS, by the assessment of several hallmarks of aging in HGPS in vitro: senescence, proteostasis, mitochondrial function and genostability. Strikingly, BHB improved these hallmarks. Additionally, we observed a decrease in progerin, the cause of premature aging in HGPS. Further, we determinate that this effect was carried out via ULK1-mTORC1 autophagy activation.  Now, we are working on demonstrate this BHB effect in progeroid mice as well as in aged mice models focusing on heart function and histopathology.

Eduardo Monterrubio completed the bachelor degree in the University of Guadalajara, there he studied the therapeutical effect of cannabinoid receptor type 2 agonist on Parkinson mouse model. The he moves to Mexico City to conclude his Master an PhD degrees (concluded on 2021 with 29 years old), where he conducted approaches on neuronal differentiation as well as mitochondrial function in HGPS in vitro model.  Now he is working on UNAM, making studies about the mechanism and new therapeutical approaches for aging and HGPS. So far, he has published 4 papers and 1 book chapter and achieved 20 cites.