Tag: heart (Page 6 of 8)

p38? and p38? regulate postnatal cardiac metabolism through glycogen synthase 1

23/11/2021 / Sabio lab

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 p38? and p38? stress-activated protein kinases in the heart.

Cardiac fibrosis (Image: Ayelén Santamans/CNIC).

We demonstrate that p38?/? contribute to the early postnatal cardiac metabolic switch through inhibitory phosphorylation of glycogen synthase 1 (GYS1) and glycogen metabolism inactivation. Premature induction of p38?/? 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 p38?/? 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.

PLoS Biol 2021: 19 (11): e3001447.

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

13/10/2021 / Sabio lab

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 p38?; 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.

CICERONE program 2019 for Masters and advanced undergraduate students

26/02/2019 / Sabio lab

As in previous years, our group is open to master and advanced undergraduate students for extending their scientific training through hands-on experience in our laboratory during the summer recess (1 July – 30 September). In addition to carrying out a supervised research project, the students will also attend CNIC seminars.

The aim of the CICERONE program is to give university students first-hand knowledge of biomedical research so that they can make more informed choices about the possibility of pursuing a scientific career.

To apply, you must register at CNIC website before 15 April 2019.

Link	Size
2019 Guidelines	348 KB
Document of acceptance	1.53 MB
Call extract from BOE	171 KB

For the 2019 call, we are offering the following research projects:

Role of p38MAPK in metabolic diseases: Metabolic syndrome is a medical disorder defined by the co?occurrence of obesity, impaired glucose tolerance, dyslipidemia and hypertension. Stress activated protein kinases have been shown to control both obesity by itself and diabetes associated to obesity. These stress kinases are activated by several MAPK activated kinases (MKK). We want to investigate the role of MKK3 in this process and the molecular mechanism by which this kinase could affect diabetes.
p38MAPK in heart physiology: The p38MAPK pathway transduces a variety of extracellular signals regulating cellular responses to stress, being implicated in cell proliferation, differentiation and apoptosis. Its implication in the development of human diseases it is being deeply studied. Four p38MAPK family members have been identified: p38?, ?, ? and ?. Preliminary data from our laboratory show that these kinases may control cytokine production during acute and chronic inflammatory processes. Moreover, studies with genetically modified mice made in our laboratory confirm that p38MAPKs have a role in the development of the heart. Our main objective is to determine if the regulation of the p38MAPK signalling pathway could have beneficial effects in the cardiac response to exercise.