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Tag: p38γ (Page 1 of 5)

p38γ and p38δ regulate postnatal cardiac metabolism through glycogen synthase 1

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.

Cardiac fibrosis (Image: Ayelén Santamans/CNIC).

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.

Entrevista a Guadalupe Sabio y Antonia Tomás, ganadoras del Premio de Investigación Fundación Dr. Antoni Esteve 2021

“Lo que nosotros descubrimos es que p38gamma se activa cuando la célula tiene un estrés. Ese estrés, en algunos casos, es un desencadenante de cáncer hepático ya que va a producir un aumento de la proliferación celular, es decir, que las células se empiecen a multiplicar. Es esa p38gamma que se activa la que controla la proliferación celular, ese aumento del número de células que al final va a desencadenar un tumor”.

Guadalupe Sabio (dcha.) y Antonia Tomás-Loba.

EMBO e-talks: Stress kinases in cardiometabolic diseases (3 Nov 2021)

On Wednesday 3 Novmber 2021 al 14:00 (CET), Guadalupe Sabio will talk at an EMBO e-talk about the role of stress kinases in cardiometabolic diseases.

To attend the talk yu should register at the following link: https://embo-org.zoom.us/webinar/register/WN_ePJby4iNRbyj0oSxxtgDUQ

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.

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