Cited by 97Cardiac Fibrosis and RemodelingCardiovascular Function and Risk FactorsAdipokines, Inflammation, and Metabolic Diseases

Leptin induces elongation of cardiac myocytes and causes eccentric left ventricular dilatation with compensation

Abe, Yukiko, Ono, Koh, Kawamura, Teruhisa, Wada, Hiromichi, Kita, Toru, Shimatsu, Akira, Hasegawa, Koji·2007·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

One of the major manifestations of obesity is an increased production of the adipocyte-derived 16-kDa peptide leptin, which acts mainly on hypothalamic leptin receptors. Leptin receptors are widely distributed in various tissues, including the heart. Whereas increased plasma leptin levels have been reported in patients with congestive heart failure, systemic alterations induced by obesity can affect cardiac hypertrophy, and the direct effects of leptin on cardiac structure and function still remain to be determined. We first exposed primary cardiac myocytes from neonatal rats to leptin for 48 h. This resulted in a significant increase in myocyte long-axis length ( P < 0.05 at 50 ng/ml) but not in the short-axis width. Leptin induced the rapid phosphorylation of STAT3 and its DNA binding in cardiac myocytes. Administration of a JAK2 inhibitor, AG-490, completely inhibited all of these effects by leptin. Furthermore, we examined the effect of continuous infusion of leptin for 4 wk following myocardial infarction in mice. Echocardiography demonstrated that left ventricular fractional shortening in the leptin-infused group (28.4 ± 2.8%) was significantly higher than that in the PBS-infused group (18.4 ± 2.2%) following myocardial infarction. Interestingly, left ventricular diastolic dimension in the leptin-infused group (4.56 ± 0.12 mm) was also higher than that in the PBS-infused group (4.13 ± 0.09 mm). These results demonstrate that leptin induces the elongation of cardiac myocytes via a JAK/STAT pathway and chronic leptin infusion causes eccentric dilatation with augmented systolic function after myocardial infarction.

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Crossref · 10.1152/ajpheart.00579.2006

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  • Leptin administration has been shown to reduce infarct size and enhance myocardial functional recovery following coronary artery ligation in mice.

    “Thus leptin administration has been shown to reduce infarct size and enhance myocardial functional recovery following coronary artery ligation in mice (4, 326).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [4]

  • Leptin administration in mice has been shown to reduce infarct size and enhance functional recovery following coronary artery ligation.

    “Notably, leptin administration in mice has been shown to reduce infarct size and enhance functional recovery following coronary artery ligation (4, 326).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [4]

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Authors
Abe, Y., Ono, K., Kawamura, T., Wada, H., Kita, T., Shimatsu, A., & Hasegawa, K.
Affiliations
Kyoto University (JP)
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2007-05
Volume
292
Issue
5
Pages
H2387-H2396
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2165799170
Cited by
97
References
31
Citations by year
2026: 2 · 2025: 6 · 2024: 4 · 2023: 1 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 5 · 2013: 6 · 2012: 11
FWCI
5.62
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
leptin, cardiac compensation, STAT3 phosphorylation, JAK2 signaling, myocardial infarction, obesity, congestive heart failure, cardiac hypertrophy, leptin receptor
MeSH terms
Animals, Animals, Newborn, Cells, Cultured, Dose-Response Relationship, Drug, Rats, Sprague-Dawley, Hypertrophy, Left Ventricular, Leptin, Myocytes, Cardiac, Cell Size, Rats

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