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Cardiovascular Research Advance Access originally published online on October 30, 2007
Cardiovascular Research 2008 77(1):4-5; doi:10.1093/cvr/cvm053
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Leptin-induced cardiac hypertrophy: RhoAing a lipid raft down a protective p38 MAPK signalling stream?

Chris J. Pemberton

Christchurch Cardioendocrine Research Group, University of Otago, 21 St Asaph Street, Christchurch 8140, New Zealand

Correspondence author. Tel: +643 364 0887; fax: +643 364 0818.E-mail address: chris.pemberton@chmeds.ac.nz

Editorial commentary on ‘Leptin-induced cardiomyocyte hypertrophy involves selective caveolae and RhoA/ROCK dependent p38 MAPK translocation to nuclei’ (Zeidan et al., pp. 64–72) and ‘Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury’ (McGaffin et al., pp. 54–63).

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The 16-kDa peptide leptin has multiple physiological actions that affect satiety, energy expenditure, reproduction, immunity, and the cardiovascular system. These actions are mediated via the Ob-R receptor system, which has six isoforms (a–f) and are distributed widely throughout the body. The major contributor to circulating concentrations of leptin (~5–15 ng/mL in lean humans) is adipose tissue secretion, and as such, leptin has been vigorously studied as part of the physiological adipose tissue hormonal signalling pathway controlling appetite, energy balance, and obesity.1 However, over recent years it has become clear that leptin is not exclusively produced by adipocytes and that organs such as the heart have their own endogenous leptin signalling systems. Thus, cardiomyocytes synthesise and secrete leptin . . . [Full Text of this Article]


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Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury
Kenneth R. McGaffin, Cheuk-Kwan Sun, Jennifer J. Rager, Lia C. Romano, Baobo Zou, Michael A. Mathier, Robert M. O'Doherty, Charles F. McTiernan, and Christopher P. O'Donnell
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