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Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies

Epicardial adipose tissue (EAT) is located between the myocardium and visceral pericardium. The unique anatomy and physiology of the EAT determines its great potential in locally influencing adjacent tissues such as the myocardium and coronary arteries. Classified by research methodologies, this stu...

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Autores principales: Song, Yujie, Tan, Yanzhen, Deng, Meng, Shan, Wenju, Zheng, Wenying, Zhang, Bing, Cui, Jun, Feng, Lele, Shi, Lei, Zhang, Miao, Liu, Yingying, Sun, Yang, Yi, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10594046/
https://www.ncbi.nlm.nih.gov/pubmed/37881786
http://dx.doi.org/10.1002/mco2.413
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author Song, Yujie
Tan, Yanzhen
Deng, Meng
Shan, Wenju
Zheng, Wenying
Zhang, Bing
Cui, Jun
Feng, Lele
Shi, Lei
Zhang, Miao
Liu, Yingying
Sun, Yang
Yi, Wei
author_facet Song, Yujie
Tan, Yanzhen
Deng, Meng
Shan, Wenju
Zheng, Wenying
Zhang, Bing
Cui, Jun
Feng, Lele
Shi, Lei
Zhang, Miao
Liu, Yingying
Sun, Yang
Yi, Wei
author_sort Song, Yujie
collection PubMed
description Epicardial adipose tissue (EAT) is located between the myocardium and visceral pericardium. The unique anatomy and physiology of the EAT determines its great potential in locally influencing adjacent tissues such as the myocardium and coronary arteries. Classified by research methodologies, this study reviews the latest research progress on the role of EAT in cardiovascular diseases (CVDs), particularly in patients with metabolic disorders. Studies based on imaging techniques demonstrated that increased EAT amount in patients with metabolic disorders is associated with higher risk of CVDs and increased mortality. Then, in‐depth profiling studies indicate that remodeled EAT may serve as a local mediator of the deleterious effects of cardiometabolic conditions and plays a crucial role in CVDs. Further, in vitro coculture studies provided preliminary evidence that the paracrine effect of remodeled EAT on adjacent cardiomyocytes can promote the occurrence and progression of CVDs. Considering the important role of EAT in CVDs, targeting EAT might be a potential strategy to reduce cardiovascular risks. Several interventions have been proved effective in reducing EAT amount. Our review provides valuable insights of the relationship between EAT, metabolic disorders, and CVDs, as well as an overview of the methodological constructs of EAT‐related studies.
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spelling pubmed-105940462023-10-25 Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies Song, Yujie Tan, Yanzhen Deng, Meng Shan, Wenju Zheng, Wenying Zhang, Bing Cui, Jun Feng, Lele Shi, Lei Zhang, Miao Liu, Yingying Sun, Yang Yi, Wei MedComm (2020) Reviews Epicardial adipose tissue (EAT) is located between the myocardium and visceral pericardium. The unique anatomy and physiology of the EAT determines its great potential in locally influencing adjacent tissues such as the myocardium and coronary arteries. Classified by research methodologies, this study reviews the latest research progress on the role of EAT in cardiovascular diseases (CVDs), particularly in patients with metabolic disorders. Studies based on imaging techniques demonstrated that increased EAT amount in patients with metabolic disorders is associated with higher risk of CVDs and increased mortality. Then, in‐depth profiling studies indicate that remodeled EAT may serve as a local mediator of the deleterious effects of cardiometabolic conditions and plays a crucial role in CVDs. Further, in vitro coculture studies provided preliminary evidence that the paracrine effect of remodeled EAT on adjacent cardiomyocytes can promote the occurrence and progression of CVDs. Considering the important role of EAT in CVDs, targeting EAT might be a potential strategy to reduce cardiovascular risks. Several interventions have been proved effective in reducing EAT amount. Our review provides valuable insights of the relationship between EAT, metabolic disorders, and CVDs, as well as an overview of the methodological constructs of EAT‐related studies. John Wiley and Sons Inc. 2023-10-24 /pmc/articles/PMC10594046/ /pubmed/37881786 http://dx.doi.org/10.1002/mco2.413 Text en © 2023 The Authors. MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Reviews
Song, Yujie
Tan, Yanzhen
Deng, Meng
Shan, Wenju
Zheng, Wenying
Zhang, Bing
Cui, Jun
Feng, Lele
Shi, Lei
Zhang, Miao
Liu, Yingying
Sun, Yang
Yi, Wei
Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
title Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
title_full Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
title_fullStr Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
title_full_unstemmed Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
title_short Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
title_sort epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10594046/
https://www.ncbi.nlm.nih.gov/pubmed/37881786
http://dx.doi.org/10.1002/mco2.413
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