Show simple item record

dc.contributor.authorLeiva, Magdalena 
dc.contributor.authorMatesanz, Nuria 
dc.contributor.authorPulgarin-Alfaro, Marta 
dc.contributor.authorNikolic, Ivana 
dc.contributor.authorSabio, Guadalupe 
dc.date.accessioned2021-07-15T11:21:27Z
dc.date.available2021-07-15T11:21:27Z
dc.date.issued2020-12
dc.identifier.citationFront Endocrinol (Lausanne). 2020; 11:572089es_ES
dc.identifier.issn1664-2392es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13244
dc.description.abstractThe 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. 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.es_ES
dc.description.sponsorshipML was supported by a Spanish grant MINECO-FEDERSAF2015- 74112-JIN and Fundación AECC: INVES20026LEIV. MP was a fellow of the Spanish State programme for the Promotion of Talent and its Employment (PRE2018-083631). IN was funded by the EFSD/Lilly grants (2017 and 2019), the CNIC IPP FP7 Marie Curie Programme (PCOFUND-2012-600396), an EFSD Rising Star award (2019), and the JDC-2018-Incorporación (MIN/JDC1802). GS received funding from the following programs and organizations: European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement n° ERC 260464, the EFSD/Lilly European Diabetes Research Programme, the BBVA Foundation Leonardo Grants program for Researchers and Cultural Creators (Investigadores-BBVA-2017) IN[17]_BBM_BAS_0066, MINECO-FEDER SAF2016-79126-R, and the Comunidad de Madrid (IMMUNOTHERCAN-CM S2010/BMD-2326 and B2017/BMD-3733). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia, Innovación y Universidades (MCNU), and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (SEV-2015-0505).es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Media es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshAdipogenesis es_ES
dc.subject.meshAdipose Tissue es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCell Plasticity es_ES
dc.subject.meshCell Transdifferentiation es_ES
dc.subject.meshHumans es_ES
dc.subject.meshInflammation es_ES
dc.subject.meshThermogenesis es_ES
dc.subject.meshp38 Mitogen-Activated Protein Kinases es_ES
dc.titleUncovering the Role of p38 Family Members in Adipose Tissue Physiology.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33424765es_ES
dc.format.volume11es_ES
dc.format.page572089es_ES
dc.identifier.doi10.3389/fendo.2020.572089es_ES
dc.contributor.funderMinisterio de Ciencia e Innovación (España) 
dc.contributor.funderFundación Lilly 
dc.contributor.funderUnión Europea. Comisión Europea. H2020 
dc.contributor.funderUnión Europea 
dc.contributor.funderFundación BBVA 
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España) 
dc.contributor.funderFundación ProCNIC 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fendo.2020.572089es_ES
dc.identifier.journalFrontiers in endocrinologyes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Papel de las quinasas activadas por el estrés en el desarrollo de enfermedades cardiovasculares, diabetes y cánceres_ES
dc.repisalud.institucionCNICes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/PCOFUND-2012-600396es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/FP7/2007-2013es_ES
dc.rights.accessRightsopen accesses_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PRE2018-083631es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/MIN/JDC1802es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/IN[17]_BBM_BAS_0066es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SAF2016-79126-Res_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/S2010/BMD-2326es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/B2017/BMD-3733es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES


Files in this item

Acceso Abierto
Thumbnail

This item appears in the following Collection(s)

Show simple item record

Atribución 4.0 Internacional
This item is licensed under a: Atribución 4.0 Internacional