We are seeking a highly motivated candidate, who would like to start a scientific career doing their doctoral thesis working in understanding the molecular mechanisms involved in how metabolic alterations can affect the cardiac disease, focusing on cardiac metabolism and how the rest of the organs affect it. This work will be supervised by Dr. Guadalupe Sabio.
We offer incorporation to CNIC via an FPU predoctoral contract (FPU 2021 call).
This call is open to applicants from all nationalities holding a Master’s degree in Biomedical Sciences and an academic record with average grade over 8,7 (out of 10).
An excellent academic record and previous research experience during their undergraduate period will be valued very positively.
Authorship of publicacions in indexed journal will be valued very positively.
Candidates must have a solid working knowledge of English.
If you are interested, please send your CV, academic record, a letter of interest and contact details of previous references to Laura Grau (email@example.com) indicating in the subject: “FPU2021 Guadalupe Sabio’s lab” no later than December 7th 2021.
Interested candidates will also need to apply officially throught the official governmental application for this predoctoral program (additional information: FPU 2021 call ).
Ayelén M. Santamans, Valle Montalvo-Romeral, Alfonso Mora, Juan Antonio Lopez, Francisco González-Romero, Daniel Jimenez-Blasco, Elena Rodríguez, Aránzazu Pintor-Chocano, Cristina Casanueva-Benítez, Rebeca Acín-Pérez, Luis Leiva-Vega, Jordi Duran, Joan J. Guinovart, Jesús Jiménez-Borreguero, José Antonio Enríquez, María Villlalba-Orero, Juan P. Bolaños, Patricia Aspichueta, Jesús Vázquez, Bárbara González-Terán, Guadalupe Sabio.
During the first weeks of postnatal heart development, cardiomyocytes undergo a major adaptive metabolic shift from glycolytic energy production to fatty acid oxidation. This metabolic change is contemporaneous to the up-regulation and activation of the p38γ and p38δ stress-activated protein kinases in the heart.
We demonstrate that p38γ/δ contribute to the early postnatal cardiac metabolic switch through inhibitory phosphorylation of glycogen synthase 1 (GYS1) and glycogen metabolism inactivation. Premature induction of p38γ/δ activation in cardiomyocytes of newborn mice results in an early GYS1 phosphorylation and inhibition of cardiac glycogen production, triggering an early metabolic shift that induces a deficit in cardiomyocyte fuel supply, leading to whole-body metabolic deregulation and maladaptive cardiac pathogenesis. Notably, the adverse effects of forced premature cardiac p38γ/δ activation in neonate mice are prevented by maternal diet supplementation of fatty acids during pregnancy and lactation.
These results suggest that diet interventions have a potential for treating human cardiac genetic diseases that affect heart metabolism.
The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. There are four different p38 family members with different roles in relation to cardiac development and function.
The first isoform demonstrated to play an important role in cardiac development was p38α; however, all p38 family members are now known to collaborate in different aspects of cardiomyocyte differentiation and growth. p38 family members have been proposed to have protective and deleterious actions in the stressed myocardium, with the outcome of their action dependent on the model system under study and the identity of the p38 family member activated.
In this talk, we summarize current understanding of the role of the p38 pathway in cardiac physiology and discuss recent advances in the field.