Cargando…

Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws

Metabolic syndrome and its component phenotypes, hyperglycemia, hypertension, (abdominal) obesity and hypertriglyceridemia, are major risk factors for atherosclerosis. Recently, associations between exposure to endocrine‐disrupting chemicals (EDCs), mitochondrial dysfunction, metabolic syndrome and...

Descripción completa

Detalles Bibliográficos
Autores principales: Lee, Hong Kyu, Shim, Eun Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wiley-Blackwell 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019282/
https://www.ncbi.nlm.nih.gov/pubmed/24843625
http://dx.doi.org/10.1111/jdi.12048
_version_ 1782480152047910912
author Lee, Hong Kyu
Shim, Eun Bo
author_facet Lee, Hong Kyu
Shim, Eun Bo
author_sort Lee, Hong Kyu
collection PubMed
description Metabolic syndrome and its component phenotypes, hyperglycemia, hypertension, (abdominal) obesity and hypertriglyceridemia, are major risk factors for atherosclerosis. Recently, associations between exposure to endocrine‐disrupting chemicals (EDCs), mitochondrial dysfunction, metabolic syndrome and atherosclerosis have been established, suggesting a possible common mechanism underlying these phenomena. Extending a previously proposed mitochondria dysfunction theory of metabolic syndrome and using biophysical laws, such as metabolic scaling, Murray's law and fractal geometry of the vascular branching system, we propose that atherosclerosis could be explained as an ill‐adaptive change occurring in nutrient‐supplying arteries in response to the decreasing tissue energy demand caused by tissue mitochondrial dysfunction. Various aspects of this new hypothesis are discussed.
format Online
Article
Text
id pubmed-4019282
institution National Center for Biotechnology Information
language English
publishDate 2013
publisher Wiley-Blackwell
record_format MEDLINE/PubMed
spelling pubmed-40192822014-05-19 Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws Lee, Hong Kyu Shim, Eun Bo J Diabetes Investig Review Articles Metabolic syndrome and its component phenotypes, hyperglycemia, hypertension, (abdominal) obesity and hypertriglyceridemia, are major risk factors for atherosclerosis. Recently, associations between exposure to endocrine‐disrupting chemicals (EDCs), mitochondrial dysfunction, metabolic syndrome and atherosclerosis have been established, suggesting a possible common mechanism underlying these phenomena. Extending a previously proposed mitochondria dysfunction theory of metabolic syndrome and using biophysical laws, such as metabolic scaling, Murray's law and fractal geometry of the vascular branching system, we propose that atherosclerosis could be explained as an ill‐adaptive change occurring in nutrient‐supplying arteries in response to the decreasing tissue energy demand caused by tissue mitochondrial dysfunction. Various aspects of this new hypothesis are discussed. Wiley-Blackwell 2013-01-29 2013-01-29 /pmc/articles/PMC4019282/ /pubmed/24843625 http://dx.doi.org/10.1111/jdi.12048 Text en Copyright © 2013 Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd
spellingShingle Review Articles
Lee, Hong Kyu
Shim, Eun Bo
Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
title Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
title_full Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
title_fullStr Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
title_full_unstemmed Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
title_short Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
title_sort extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019282/
https://www.ncbi.nlm.nih.gov/pubmed/24843625
http://dx.doi.org/10.1111/jdi.12048
work_keys_str_mv AT leehongkyu extensionofthemitochondriadysfunctionhypothesisofmetabolicsyndrometoatherosclerosiswithemphasisontheendocrinedisruptingchemicalsandbiophysicallaws
AT shimeunbo extensionofthemitochondriadysfunctionhypothesisofmetabolicsyndrometoatherosclerosiswithemphasisontheendocrinedisruptingchemicalsandbiophysicallaws