List of Titles

Quick View

Cardiac response to exercise in normal ageing : What can we learn from masters athletes?

- Beaumont, Alexander, Campbell, Amy, Grace, Fergal, Sculthorpe, Nicholas

Authors: Beaumont, Alexander , Campbell, Amy , Grace, Fergal , Sculthorpe, Nicholas
Date: 2018
Type: Text , Journal article , Review
Relation: Current Cardiology Reviews Vol. 14, no. 4 (2018), p. 245-253
Full Text:
Reviewed:
Description: Background: Ageing is associated with an inexorable decline in cardiac and vascular function, resulting in an increased risk of Cardiovascular Disease (CVD). Lifestyle factors such as exercise have emerged as a primary therapeutic target in the prevention of CVD, yet older individuals are frequently reported as being the least active, with few meeting the recommended physical activity guidelines. In contrast, well trained older individuals (Masters athletes) have superior functional capacity than their sedentary peers and are often comparable with young non-athletes. Therefore, the 'masters' athlete may be viewed as a unique non-pharmacological model which may allow researchers to disentangle the inexorable from the preventable and the magnitude of the unavoidable 'true' reduction in cardiac function due to ageing. Conclusion: This review examines evidence from studies which have compared cardiac structure and function in well trained older athletes, with age-matched controls but otherwise healthy. © 2018 Bentham Science Publishers.

Quick View

Coronary artery disease : Why we should consider the Y chromosome

- Molina, Elsa, Clarence, Elyse, Ahmady, Farah, Chew, Guatsiew, Charchar, Fadi

Authors: Molina, Elsa , Clarence, Elyse , Ahmady, Farah , Chew, Guatsiew , Charchar, Fadi
Date: 2016
Type: Text , Journal article , Review
Relation: Heart Lung and Circulation Vol. 25, no. 8 (Aug 2016), p. 791-801
Relation: http://purl.org/au-research/grants/nhmrc/1009490
Full Text:
Reviewed:
Description: Coronary artery disease (CAD) is one of the leading causes of morbidity and mortality globally. In the last few years our understanding of the genetic and molecular mechanisms that promote CAD in individuals has increased with the advent of the genome era. This complex inflammatory disease has well-defined environmental risk factors. However, in the last 10 years, studies including genome-wide association studies (GWAS) have clearly demonstrated a genetic influence on CAD. Recently, studies on the human Y chromosome have also demonstrated that genetic variation within the male-specific region of the Y chromosome (MSY) could play a part in determining cardiovascular risk in men, confirming the notion that the increased risk for CAD in men cannot be fully explained through common CAD risk factors. Here, we review the literature about the pathophysiology of CAD, its potential causes and environmental risk factors known so far. Furthermore, we review the genetics of CAD, especially the latest discoveries regarding the implication of the Y chromosome, the most underexplored portion of the human genome to date, highlighting methods and difficulties arising in this research field, and discussing the importance of considering the Y chromosome in CAD research.

Dysregulation of c-kit expression parallels the development of spontaneous genetic cardiac hypertrophy

- Marques, Francine, Prestes, Priscilla, Lewandowski, Paul, Harrap, Stephen, Charchar, Fadi

Authors: Marques, Francine , Prestes, Priscilla , Lewandowski, Paul , Harrap, Stephen , Charchar, Fadi
Date: 2015
Type: Text , Conference paper
Relation: Cardiac Society of Australia and New Zealand Annual Scientific Meeting and the International Society for Heart Research Australasian Section Annual Scientific Meeting; Melbourne, Victoria, Australia; 13th-16th August 2016; published in Heart, Lung and Circulation. Vol. 24, p. S401-S401
Full Text: false
Reviewed:
Description: Objective: The molecular processes associated with cardiac hypertrophy independent of blood pressure are still largely unknown. The hypertrophic heart rate (HHR) is normotensive and born with a reduced complement of cardiomyocytes that predisposes to cardiac hypertrophy and failure in later life. We investigated the expression of c-kit gene, a marker of cardiac stem cells and myocardial regeneration that could contribute to hypertrophy. Methods: Left ventricular c-kit mRNA expression was measured by real-time PCR in HHR and control strain in neonatal and 38-week old rats (n=7-12/group). We tested for linkage of c-kit expression with neonatal cardiac size in 197 second generation crosses (F2) of HHR and control strain. Results: c-kit mRNA was slightly up-regulated in neonatal (fold change +1.3, P=0.02) and markedly so in 38-week old HHR (+35.5, P=0.0003). Cardiac weight index was positively correlated with neonatal myocardial c-kit mRNA in the F2 population (r=0.19, P=0.007). Conclusions: In HHR hearts c-kit expression appears increased throughout life, but more so in the adult where cardiac hypertrophy is established and leading to failure. In aged hypertrophic hearts, over-expression of c-kit is likely a compensatory mechanism of the failing heart. Previous studies showed an activation of cardiac stem cells in the hypertrophic myocardium. Our study suggests that c-kit might be involved from an early age in mechanisms that lead to cardiac hypertrophy in adulthood.

Quick View

Cardiovascular risk and androgenic anabolic steroids

- Sculthorpe, Nicholas, Grace, Fergal, Angell, Peter, Baker, Julien, George, Keith

Authors: Sculthorpe, Nicholas , Grace, Fergal , Angell, Peter , Baker, Julien , George, Keith
Date: 2013
Type: Text , Journal article
Relation: British Journal of Cardiac Nursing Vol. 7, no. 6 (2013), p. 266-275
Full Text: false
Reviewed:
Description: Although several drugs are purported to improve exercise performance, androgenic anabolic steroids (AAS) are the most widespread. Furthermore, unlike other drugs, their use has expanded beyond competition, to non-competitive and recreational athletes. Correspondingly health professionals are more likely to come into contact with users of AAS than with users of other performance-enhancing drugs. While there are numerous reports outlining serious cardiovascular consequences to high-dose AAS abuse, this evidence is often limited by difficulties in gaining access to users due to the legal status of AAS. Additionally the co-abuse of other substances (as additional muscle mass enhancers, or to mitigate possible side effects) is a further confounding factor. This review examines the evidence for AAS having a negative effect on the cardiac and vascular tissue and the corresponding risk of developing cardiovascular disease. Possible mechanisms of action by which AAS bring about these changes are also discussed.

Abnormal microRNA expression in cardiac hypertrophy and the regulation of the Endog gene

- Quarrell, Sean, Marques, Francine, Jayaswal, Vivek, Curl, Claire, Nankervis, Scott, Yang, Jean, Delbridge, Lea, Harrap, Stephen, Charchar, Fadi

Authors: Quarrell, Sean , Marques, Francine , Jayaswal, Vivek , Curl, Claire , Nankervis, Scott , Yang, Jean , Delbridge, Lea , Harrap, Stephen , Charchar, Fadi
Date: 2012
Type: Text , Journal article
Relation: Heart, Lung and Circulation Vol. 21, no. Supplement 1 (2012), p. s7
Full Text: false
Reviewed:
Description: A deficiency in the gene for endonuclease G (Endog) was recently described as a genetic determinant of cardiac hypertrophy. The mechanisms involved in the regulation of Endog, however, are still to be elucidated. Therefore we hypothesised that Endog, being regulated by small regulatory non-coding RNAs called microRNAs (miRNAs), could contribute to the cardiac hypertrophy of the Hypertrophic Heart Rat (HHR), a human polygenic model of cardiac hypertrophy. From birth the HHR has less and smaller cardiomyocytes, which leads to hypertrophy and cardiac failure later in life. In this study, we examined genome-wide miRNA expression by Agilent Rat miRNA Microarray Kit Release 16.0 and Endog mRNA levels by real-time PCR in the left ventricle of neonatal HHR compared to age-matched rats from its authentic control, the Normal Heart Rat (NHR). Endog mRNA was significantly under-expressed in the HHR (fold change=−4.7; P=0.0001). Sixty-seven miRNAs (FDR P<0.05 and fold change>1.1) were differentially expressed between HHR and NHR (n=16). We then performed an in silico analysis to predict the miRNAs that are able to bind to the 3′ untranslated region of Endog mRNA, and therefore could regulate Endog levels. We discovered that the miRNAs let-7b, miR-338 and miR-347 are predicted to bind to Endog mRNA. Functional studies are being undertaken to determine whether these miRNAs can regulate Endog mRNA levels in vitro and their role in the pathological processes leading to cardiac hypertrophy. These miRNAs could be a new target for the prevention and treatment of cardiac hypertrophy in humans

Showing items 1 - 8 of 8