Oxidative Stress and Heart F... [Am J Physiol Heart Circ Physiol. 2011] - PubMed - NCBI

Am J Physiol Heart Circ Physiol. 2011 Sep 23. [Epub ahead of print]
Oxidative Stress and Heart Failure.

Tsutsui H, Kinugawa S, Matsushima S.
Source

1Hokkaido University Graduate School of Medicine.

Abstract

Oxidative stress, defined as an excess production of reactive oxygen species (ROS) relative to antioxidant defense, has been shown to play an important role in the pathophysiology of cardiac remodeling and heart failure (HF). It induces subtle changes in intracellular pathways, redox signaling, at lower levels, but causes cellular dysfunction and damage at higher levels. ROS are derived from several intracellular sources including mitochondria, NAD(P)H oxidase, xanthine oxidase, and uncoupled nitric oxide synthase. The production of ROS is increased within the mitochondria from failing hearts whereas normal antioxidant enzyme activities are preserved. Chronic increases in ROS production in the mitochondria lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further ROS generation, and cellular injury. ROS directly impair contractile function by modifying proteins central to excitation-contraction coupling. Moreover, ROS activate a broad variety of hypertrophy signaling kinases and transcription factors and mediate apoptosis. They also stimulate cardiac fibroblast proliferation and activate the matrix metalloproteinases, leading to the extracellular matrix remodeling. These cellular events are involved in the development and progression of maladaptive myocardial remodeling and failure. Oxidative stress is also involved in the skeletal muscle dysfunction, which may be associated with exercise intolerance and insulin resistance in HF. Therefore, oxidative stress is involved in the pathophysiology of HF in the heart as well as in the skeletal muscle. A better understanding of these mechanisms may enable the development of novel and effective therapeutic strategies against HF.


PMID:21949114 [PubMed - as supplied by publisher]

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"Oxidative stress, defined as an excess production of reactive oxygen species (ROS) relative to antioxidant defense"

This means that taking something that boosts our bodies own endogenous antioxidants such as glutathione, sod and catalase so that the excess ROS produced by the mitochondria of someone in poor health could bring those ROS levels down so that there is a relief in the oxidative stress.