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The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium

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datacite.rightshttp://purl.org/coar/access_right/c_abf2eng
dc.contributor.authorBermúdez, Valmore
dc.contributor.authorDurán, Pablo
dc.contributor.authorRojas, Edward
dc.contributor.authorDíaz, María P.
dc.contributor.authorRivas, José
dc.contributor.authorNava, Manuel
dc.contributor.authorChací, Maricarmen
dc.contributor.authorCabrera de Bravo, Mayela
dc.contributor.authorCarrasquero, Rubén
dc.contributor.authorCano Ponce, Clímaco
dc.contributor.authorGórriz, José Luis
dc.contributor.authorD'Marco, Luis
dc.date.accessioned2021-10-06T15:17:08Z
dc.date.available2021-10-06T15:17:08Z
dc.date.issued2021
dc.description.abstractAdipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen in the human obese phenotype. These processes promote an abnormal adipocyte proteomic reprogramming, whereby these cells become a source of abnormal signals, affecting vascular and myocardial tissues, leading to meta-inflammation, atrial fibrillation, coronary artery disease, heart hypertrophy, heart failure and myocardial infarction. This review first discusses the pathophysiology and consequences of adipose tissue expansion, particularly their association with meta-inflammation and microbiota dysbiosis. We also explore the precise mechanisms involved in metabolic reprogramming in AT that represent plausible causative factors for CVD. Finally, we clarify how lifestyle changes could promote improvement in myocardiocyte function in the context of changes in AT proteomics and a better gut microbiome profile to develop effective, non-pharmacologic approaches to CVD.eng
dc.format.mimetypepdfspa
dc.identifier.citationBermúdez V, Durán P, Rojas E, Díaz MP, Rivas J, Nava M, Chacín M, Cabrera de Bravo M, Carrasquero R, Ponce CC, Górriz JL and D´Marco L (2021) The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium. Front. Endocrinol. 12:735070. doi: 10.3389/fendo.2021.735070eng
dc.identifier.doihttps://doi.org/10.3389/fendo.2021.735070
dc.identifier.issn16642392
dc.identifier.urihttps://hdl.handle.net/20.500.12442/8657
dc.language.isoengeng
dc.publisherFrontiers Mediaeng
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.accessrightsinfo:eu-repo/semantics/openAccesseng
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.sourceFrontiers in Endocrinologyeng
dc.sourceVol. 12 (2021)
dc.subjectAdipose tissueeng
dc.subjectMyocardiocyteseng
dc.subjectMicrobiotaeng
dc.subjectObesityeng
dc.subjectInflammationeng
dc.titleThe Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardiumeng
dc.type.driverinfo:eu-repo/semantics/articleeng
dc.type.spaArtículo científicospa
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