TITLE

Oxidative stress and redox signalling in cardiac hypertrophy and heart failure

AUTHOR(S)
Seddon, Mike; Looi, Yee H.; Shah, Ajay M.
PUB. DATE
August 2007
SOURCE
Heart;Aug2007, Vol. 93 Issue 8, p903
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Substantial evidence suggests the involvement of oxidative stress in the pathophysiology of congestive heart failure and its antecedent conditions such as cardiac hypertrophy and adverse remodelling after MI. Oxidative stress describes an imbalance between antioxidant defences and the production of reactive oxygen species (ROS), which at high levels cause cell damage but at lower levels induce subtle changes in intracellular signalling pathways (termed redox signalling). ROS are derived from many sources including mitochondria, xanthine oxidase, uncoupled nitric oxide synthases and NADPH oxidases. The latter enzymes are especially important in redox signalling, being implicated in the pathophysiology of hypertension and atherosclerosis, and activated by diverse pathologically relevant stimuli. We review the contribution of ROS to heart failure pathophysiology and discuss potential therapies that may specifically target detrimental redox signalling. Indeed, drugs such as ACE inhibitors and statins may act in part through such mechanisms. A better understanding of redox signalling mechanisms may enable the development of new targeted therapeutic strategies rather than the non-specific antioxidant approaches that have to date been disappointing in clinical trials.
ACCESSION #
27040530

 

Related Articles

  • Subcellular remodelling may induce cardiac dysfunction in congestive heart failure. Naranjan S. Dhalla; Harjot K. Saini-Chohan; Delfin Rodriguez-Leyva; Vijayan Elimban; Melissa R. Dent; Paramjit S. Tappia // Cardiovascular Research;Feb2009, Vol. 81 Issue 3, p429 

    It is commonly held that cardiac remodelling, represented by changes in muscle mass, size, and shape of the heart, explains the progression of congestive heart failure (CHF). However, this concept does not provide any clear information regarding the development of cardiac dysfunction in CHF....

  • Anomalous papillary muscle in hypertrophic cardiomyopathy. Alfonso, Fernando; Aragoncillo, Paloma; Alfonso, F; Aragoncillo, P // Heart;Jul2001, Vol. 86 Issue 1, p2 

    This article illustrates scanned images of a case of anomalous papillary muscle in hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy may cause congestive heart failure. Failure to recognise its predominant pathophysiologic mechanism may have adverse consequences. A 75 year old women was...

  • Genetic mutations and mechanisms in dilated cardiomyopathy. McNally, Elizabeth M.; Golbus, Jessica R.; Puckelwartz, Megan J. // Journal of Clinical Investigation;Jan2013, Vol. 123 Issue 1, p19 

    Genetic mutations account for a significant percentage of cardiomyopathies, which are a leading cause of conges-tive heart failure. In hypertrophic cardiomyopathy (HCM), cardiac output is limited by the thickened myocardium through impaired filling and outflow. Mutations in the genes encoding...

  • Role of Subcellular Remodeling in Cardiac Dysfunction due to Congestive Heart Failure. Babick, Andrea P.; Dhalla, Naranjan S. // Medical Principles & Practice;Mar2007, Vol. 16 Issue 2, p81 

    Although alterations in the size and shape of the heart (cardiac remodeling) are considered in explaining cardiac dysfunction during the development of congestive heart failure (CHF), there are several conditions including initial stages of cardiac hypertrophy, where cardiac remodeling has also...

  • Can Adiponectin Help us to Target Diastolic Dysfunction? Francisco, Catarina; Neves, João; Falcão-Pires, Inês; Leite-Moreira, Adelino // Cardiovascular Drugs & Therapy;Dec2016, Vol. 30 Issue 6, p635 

    Adiponectin is the most abundant adipokine and exhibits anti-inflammatory, antiatherogenic and antidiabetic properties. Unlike other adipokines, it inversely correlates with body weight and obesity-linked cardiovascular complications. Diastolic dysfunction is the main mechanism responsible for...

  • Diabetic Cardiomyopathy and Oxidative Stress: Role of Antioxidants. Thandavarayan, Rajarajan A.; Giridharan, Vijayasree V.; Watanabe, Kenichi; Konishi, Tetsuya // Cardiovascular & Hematological Agents in Medicinal Chemistry;2011, Vol. 9 Issue 4, p225 

    Diabetes has emerged as a major threat to worldwide health. The increasing incidence of diabetes in young individuals is particularly worrisome given that the disease is likely to evolve over a period of years. In 1972, the existence of a diabetic cardiomyopathy was proposed based on the...

  • Cardiac hypertrophy and oxidative stress: a leap of faith or stark reality? Lang, D. // Heart;Apr2002, Vol. 87 Issue 4, p316 

    This article focuses on a study related to the cardiac hypertrophy and oxidative stress. The term "oxidative stress" has become something of a buzz phrase in recent years, being implicated in countless disease processes. Given that cardiac myocyte mitochondria can generate reactive oxygen...

  • OXIDATIVE STRESS AND CARDIAC HYPERTROPHY. Maulik, S. K.; Kumar, Santosh // IIOAB Journal;Jul2011, Vol. 2 Issue 6, p107 

    In this article, the authors discuss sources of reactive oxygen species (ROS) generation in oxidative stress, which causes chronic cardiac hypertrophy (CH) development. The authors mention that ROS are produced as reduction-oxidation reaction intermediates. They mention that Nicotinamide Adenine...

  • Oxidative stress in aldosteronism. Sun, Yao; Ahokas, Robert A.; Bhattacharya, Syamal K.; Gerling, Ivan C.; Carbone, Laura D.; Weber, Karl T. // Cardiovascular Research;Jul2006, Vol. 71 Issue 2, p300 

    Abstract: Congestive heart failure (CHF) is more than a failing heart and salt-avid state. Also present is a systemic illness which features oxidative stress in diverse tissues, a proinflammatory phenotype, and a wasting of soft tissue and bone. Reactive oxygen and nitrogen species contribute to...

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics