%0 Journal Article
%T Mitochondrial Dysfunction in Metabolic Syndrome and Asthma
%A Ulaganathan Mabalirajan
%A Balaram Ghosh
%J Journal of Allergy
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/340476
%X Though severe or refractory asthma merely affects less than 10% of asthma population, it consumes significant health resources and contributes significant morbidity and mortality. Severe asthma does not fell in the routine definition of asthma and requires alternative treatment strategies. It has been observed that asthma severity increases with higher body mass index. The obese-asthmatics, in general, have the features of metabolic syndrome and are progressively causing a significant burden for both developed and developing countries thanks to the westernization of the world. As most of the features of metabolic syndrome seem to be originated from central obesity, the underlying mechanisms for metabolic syndrome could help us to understand the pathobiology of obese-asthma condition. While mitochondrial dysfunction is the common factor for most of the risk factors of metabolic syndrome, such as central obesity, dyslipidemia, hypertension, insulin resistance, and type 2 diabetes, the involvement of mitochondria in obese-asthma pathogenesis seems to be important as mitochondrial dysfunction has recently been shown to be involved in airway epithelial injury and asthma pathogenesis. This review discusses current understanding of the overlapping features between metabolic syndrome and asthma in relation to mitochondrial structural and functional alterations with an aim to uncover mechanisms for obese-asthma. 1. Introduction Mitochondria, dynamic organelles assumed to be originated from ¦Á-proteobacteria, not only generate energy in the form of ATP but also regulate numerous cellular functions relevant to cell fate, such as apoptosis, generation of oxidative free radicals, and calcium homeostasis [1]. Every mitochondrion has 2 membranous and 2 aqueous compartments: outer membrane, intermembranous space, inner membrane, and matrix [2]. Outer membrane contains numerous porins which form channels through which solutes (¡Ü5000 Daltons) enter freely inside the mitochondria. In contrast, it specifically permits larger mitochondria-targeting signal peptide containing pre-proteins which interact with translocase of outer membrane complex [3]. Mitochondrial intermembranous space, one of the aqueous compartments, contains small molecules which are very similar to cytosol, protein components which vary from cytosol thanks to the restricted entry of larger proteins through outer membrane and protons from oxidative phosphorylation [4]. The inner membrane of mitochondria is folded to form enormous cristae to increase the surface area and to enhance the ATP generating
%U http://www.hindawi.com/journals/ja/2013/340476/