IMR Press / FBE / Volume 4 / Issue 6 / DOI: 10.2741/e530

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Autophagy in the stress-induced myocardium

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1 The Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH
2 Department of Clinical Medicine, Trinity Centre for Health Sciences, St James’s Hospital, Trinity College, Dublin
3 Centre for Heart and Vessel Preclinical Studies, St John Hospital Medical Centre, Wayne State University Medical School, Detroit, MI, USA
4 Birkbeck College, University of London, Malet Street, London, WC1E 7HX

*Author to whom correspondence should be addressed.

Academic Editor: Sean Barry

Front. Biosci. (Elite Ed) 2012, 4(6), 2131–2141;
Published: 1 January 2012
(This article belongs to the Special Issue Emerging therapies in cardiovascular disease)

Cardiovascular disease is a leading cause of death worldwide, particularly in Western societies. During an ischaemic insult, ventricular pressure from the heart is diminished as a result of cardiac myocyte death by necrosis and apoptosis. Autophagy is a process whereby cells catabolise intracellular proteins in order to generate ATP in times of stress such as nutrient starvation and hypoxia. Emerging evidence suggests that autophagy plays a positive role in cardiac myocyte survival during periods of cellular stress performing an important damage limitation function. By promoting cell survival, cardiac myocyte loss is reduced thereby minimising the potential of heart failure. In contrast, it has been reported that autophagy can also be a form of cell death. By considering the various animal models of autophagy, we examine the role of the Signal Transducers and Activator of Transcription (STAT) proteins in the autophagic response. Additionally we review the role of the tumour suppressor, p53 and its family member p73 and their potential role in the autophagic response.

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