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Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction

  • Hypertension and Obesity (E Reisin, Section Editor)
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Abstract

Mitochondria are the primary generators of cellular reactive oxygen species (ROS); their pathophysiological roles in hypertension and insulin resistance are but imperfectly understood. Mitochondrial dysfunction has been linked to the etiologies of many complex diseases, but many other factors, including the upregulation of the renin-angiotensin system (RAS) and vitamin D deficiency, have also been implicated in hypertension pathogenesis. Hypertension resulting from the disruption of the RAS contributes to the risk of cardiovascular disease. Likewise, experimental and clinical evidence indicate that RAS stimulation and low vitamin D levels are inversely related and represent risk factors associated with the pathogenesis of hypertension. Furthermore, RAS activation induces insulin resistance, resulting in increases in ROS levels. High levels of ROS are harmful to cells, having the potential to trigger both mitochondrial-mediated apoptosis and the degradation of the mitochondrial DNA. Diabetes risk is also associated with high levels of oxidative stress; taking vitamin D, however, may reduce that risk. The finding that mitochondria possess both a functional RAS and vitamin D receptors is the starting point for improving our understanding of the interaction of mitochondria and chronic disease states, which understanding should lead to decreases in the chronic disease burden attributable to hypertension, diabetes, or both.

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Walter Manucha, Bob Richie, and León Ferder declare no conflicts of interest.

Human and Animal Rights and Informed Consent

The animal experiments described herein were not performed by any of the authors, signifying that no animals were harmed in the course of preparing this manuscript.

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Correspondence to Walter Manucha.

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This article is part of the Topical Collection on Hypertension and Obesity

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Manucha, W., Ritchie, B. & Ferder, L. Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction. Curr Hypertens Rep 17, 504 (2015). https://doi.org/10.1007/s11906-014-0504-2

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