Cargando…

Autophagy and cardiometabolic risk factors

Autophagy is an essential cellular pathway by which protein aggregates, long-lived proteins, or defective organelles are sequestered in double membrane vesicles and then degraded upon fusion of those vesicles with lysosomes. Although autophagy plays a critical role in maintaining intracellular homeo...

Descripción completa

Detalles Bibliográficos
Autores principales: Juárez-Rojas, Juan G., Reyes-Soffer, Gissette, Conlon, Donna, Ginsberg, Henry N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237938/
https://www.ncbi.nlm.nih.gov/pubmed/25246308
http://dx.doi.org/10.1007/s11154-014-9295-7
_version_ 1782345430002040832
author Juárez-Rojas, Juan G.
Reyes-Soffer, Gissette
Conlon, Donna
Ginsberg, Henry N.
author_facet Juárez-Rojas, Juan G.
Reyes-Soffer, Gissette
Conlon, Donna
Ginsberg, Henry N.
author_sort Juárez-Rojas, Juan G.
collection PubMed
description Autophagy is an essential cellular pathway by which protein aggregates, long-lived proteins, or defective organelles are sequestered in double membrane vesicles and then degraded upon fusion of those vesicles with lysosomes. Although autophagy plays a critical role in maintaining intracellular homeostasis and keeping the cell in a healthy state, this key pathway can become dysregulated in various cardiometabolic disorders, such as; obesity, dyslipidemia, inflammation, and insulin resistance. In these conditions, autophagy may actually worsen the pathological state instead of protecting the cell or organism. In this review, we discuss how dysregulated autophagy may be linked to increases in cardiovascular risk factors, and how manipulation of the autophagic machinery might reduce those risks.
format Online
Article
Text
id pubmed-4237938
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher Springer US
record_format MEDLINE/PubMed
spelling pubmed-42379382014-11-21 Autophagy and cardiometabolic risk factors Juárez-Rojas, Juan G. Reyes-Soffer, Gissette Conlon, Donna Ginsberg, Henry N. Rev Endocr Metab Disord Article Autophagy is an essential cellular pathway by which protein aggregates, long-lived proteins, or defective organelles are sequestered in double membrane vesicles and then degraded upon fusion of those vesicles with lysosomes. Although autophagy plays a critical role in maintaining intracellular homeostasis and keeping the cell in a healthy state, this key pathway can become dysregulated in various cardiometabolic disorders, such as; obesity, dyslipidemia, inflammation, and insulin resistance. In these conditions, autophagy may actually worsen the pathological state instead of protecting the cell or organism. In this review, we discuss how dysregulated autophagy may be linked to increases in cardiovascular risk factors, and how manipulation of the autophagic machinery might reduce those risks. Springer US 2014-09-23 2014 /pmc/articles/PMC4237938/ /pubmed/25246308 http://dx.doi.org/10.1007/s11154-014-9295-7 Text en © The Author(s) 2014 https://creativecommons.org/licenses/by/4.0/ Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Article
Juárez-Rojas, Juan G.
Reyes-Soffer, Gissette
Conlon, Donna
Ginsberg, Henry N.
Autophagy and cardiometabolic risk factors
title Autophagy and cardiometabolic risk factors
title_full Autophagy and cardiometabolic risk factors
title_fullStr Autophagy and cardiometabolic risk factors
title_full_unstemmed Autophagy and cardiometabolic risk factors
title_short Autophagy and cardiometabolic risk factors
title_sort autophagy and cardiometabolic risk factors
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237938/
https://www.ncbi.nlm.nih.gov/pubmed/25246308
http://dx.doi.org/10.1007/s11154-014-9295-7
work_keys_str_mv AT juarezrojasjuang autophagyandcardiometabolicriskfactors
AT reyessoffergissette autophagyandcardiometabolicriskfactors
AT conlondonna autophagyandcardiometabolicriskfactors
AT ginsberghenryn autophagyandcardiometabolicriskfactors