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Cited by 236Cardiac Fibrosis and RemodelingAdipokines, Inflammation, and Metabolic DiseasesCardiovascular Disease and Adiposity

The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.

Exacerbation of heart failure in adiponectin-deficient mice due to impaired regulation of AMPK and glucose metabolism

LIAO, Y, TAKASHIMA, S, MAEDA, N, OUCHI, N, KOMAMURA, K, SHIMOMURA, I, HORI, M, MATSUZAWA, Y, FUNAHASHI, T, KITAKAZE, M·2005·Cardiovascular Research
DOI 10.1016/j.cardiores.2005.04.018
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Abstract

OBJECTIVE: Insulin resistance (IR) was reported to be associated with chronic heart failure (CHF). Adiponectin, an insulin-sensitizing hormone with anti-inflammatory activity, improves energy metabolism via AMP-activated protein kinase (AMPK). AMPK deficiency is associated with depressed cardiac function under stress conditions. However, it is not clear whether adiponectin plays an important role in CHF. We hypothesize that deficiency of adiponectin might result in deterioration of heart failure. METHODS: Using adiponectin null mice and their littermates, we examined the effects of adiponectin on LV pressure overload-induced cardiac hypertrophy and failure, and investigated the mechanisms involved. RESULTS: Three weeks after transverse aortic constriction (TAC), cardiac hypertrophy (evaluated from the heart-to-body weight ratio: 7.62+/-0.27 in wild-type (WT) mice, 9.97+/-1.13 in knockout (KO) mice, P<0.05) and pulmonary congestion (lung-to-body weight ratio: 9.05+/-1.49 in WT mice, 14.95+/-2.36 in KO mice, P<0.05) were significantly greater in adiponectin KO mice than WT mice. LV dimensions were also increased in KO mice. Compared with WT TAC mice, expression of AMPKalpha protein was lower, while IR was higher in KO TAC mice. CONCLUSION: These findings indicate that adiponectin deficiency leads to progressive cardiac remodeling in pressure overloaded condition mediated via lowing AMPK signaling and impaired glucose metabolism.

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Crossref · 10.1016/j.cardiores.2005.04.018

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Metadata

Authors
LIAO, Y., TAKASHIMA, S., MAEDA, N., OUCHI, N., KOMAMURA, K., SHIMOMURA, I., HORI, M., MATSUZAWA, Y., FUNAHASHI, T., & KITAKAZE, M.
Affiliations
  • The University of Osaka (JP)
  • National Cerebral and Cardiovascular Center (JP)
Corresponding author
KITAKAZE, M
ORCID
Venue
Cardiovascular Research
Publisher
Oxford University Press (OUP)
Published
2005-09-01
Volume
67
Issue
4
Pages
705-713
ISSN
0008-6363 (ISSN-L)
DOI
10.1016/j.cardiores.2005.04.018
OpenAlex
W2148710672
Cited by
236
References
48
Citations by year
2026: 1 · 2025: 6 · 2024: 1 · 2023: 8 · 2022: 9 · 2021: 4 · 2020: 6 · 2019: 6 · 2018: 13 · 2017: 9 · 2016: 9 · 2015: 15 · 2014: 13 · 2013: 10 · 2012: 16
FWCI
13.45
Type
journal article
Language
en
Open access
closed
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords
adiponectin, heart failure, AMPK, AMPKα, insulin resistance, glucose metabolism, cardiac hypertrophy, pressure overload, transverse aortic constriction, cardiac remodeling, adiponectin knockout mice, pulmonary congestion
MeSH terms
Adenylate Kinase, Animals, Blood Glucose, Echocardiography, Fasting, Heart Failure, Insulin, Insulin Resistance, Male, Myocardium, Blotting, Western, Mice, Knockout, Mice, Adiponectin

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