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Tag: p38δ (Page 1 of 4)

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.

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:

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.

Uncovering the role of p38 family members in adipose tissue physiology

Magdalena Leiva, Nuria Matesanz, Marta Pulgarín-Alfaro, Ivana Nikolić & Guadalupe Sabio.

The complex functions of adipose tissue have been a focus of research interest over the past twenty years. Adipose tissue is not only the main energy storage depot, but also one of the largest endocrine organs in the body and carries out crucial metabolic functions. Moreover, brown and beige adipose depots are major sites of energy expenditure through the activation of adaptive, non-shivering thermogenesis.

p38-mediated adipose tissue secretome
The p38-mediated adipose tissue secretome.

In recent years, numerous signaling molecules and pathways have emerged as critical regulators of adipose tissue, in both homeostasis and obesity-related disease. Among the best characterized are members of the p38 kinase family. The activity of these kinases has emerged as a key contributor to the biology of the white and brown adipose tissues, and their modulation could provide new therapeutic approaches against obesity.

Here, we give an overview of the roles of the distinct p38 family members in adipose tissue, focusing on their actions in adipogenesis, thermogenic activity, and secretory function.

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