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 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.
Department of Internal Medicine Eulji University College of Medicine Seoul Korea.
Hong Kyu
HK
Lee
Department of Mechanical and Biomedical Engineering Kangwon National University Chuncheon Korea.
Eun Bo
EB
Shim
Atherosclerosis; Endocrine‐disrupting chemicals; Mitochondrial dysfunction