Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2–dependent mechanisms
Open accessAbstract
Obesity-related disorders are associated with the development of ischemic heart disease. Adiponectin is a circulating adipose-derived cytokine that is downregulated in obese individuals and after myocardial infarction. Here, we examine the role of adiponectin in myocardial remodeling in response to acute injury. Ischemia-reperfusion in adiponectin-deficient (APN-KO) mice resulted in increased myocardial infarct size, myocardial apoptosis and tumor necrosis factor (TNF)-alpha expression compared with wild-type mice. Administration of adiponectin diminished infarct size, apoptosis and TNF-alpha production in both APN-KO and wild-type mice. In cultured cardiac cells, adiponectin inhibited apoptosis and TNF-alpha production. Dominant negative AMP-activated protein kinase (AMPK) reversed the inhibitory effects of adiponectin on apoptosis but had no effect on the suppressive effect of adiponectin on TNF-alpha production. Adiponectin induced cyclooxygenase (COX)-2-dependent synthesis of prostaglandin E(2) in cardiac cells, and COX-2 inhibition reversed the inhibitory effects of adiponectin on TNF-alpha production and infarct size. These data suggest that adiponectin protects the heart from ischemia-reperfusion injury through both AMPK- and COX-2-dependent mechanisms.
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Administration of adiponectin diminished the infarct size, apoptosis, and TNF-α production induced by ischemia-reperfusion in both wild-type and adiponectin KO mice.
“Administration of adiponectin diminished the infarct size, apoptosis, and TNF-α production induced by ischemia-reperfusion in both wild-type and adiponectin KO mice (321).”
From Cardiac remodeling in obesity (2008) · cites this paper as [321]
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- Authors
- Shibata, R., Sato, K., Pimentel, D. R., Takemura, Y., Kihara, S., Ohashi, K., Funahashi, T., Ouchi, N., & Walsh, K.
- Affiliations
- Boston University (US)
- The University of Osaka (JP)
- Corresponding author
- Ouchi, Noriyuki
- Walsh, Kenneth
- Venue
- Nature Medicine
- Published
- 2005-09-11
- Volume
- 11
- Issue
- 10
- Pages
- 1096-1103
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC2828682
- OpenAlex
- W2027589607
- Cited by
- 982
- References
- 51
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 21 · 2023: 23 · 2022: 21 · 2021: 26 · 2020: 58 · 2019: 36 · 2018: 33 · 2017: 37 · 2016: 48 · 2015: 58 · 2014: 60 · 2013: 59 · 2012: 80
- FWCI
- 35.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association
- Uehara Memorial Foundation
- National Institutes of Health
- Japan Society for the Promotion of Science
- National Institute on Aging (R01AG015052, R37AG015052, AG15052)
- National Heart, Lung, and Blood Institute (HL-07224, HL77774, HL-66957, T32HL007224, P01HL066957, R01HL077774)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-40197, R01AR040197)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- adiponectin, myocardial ischemia-reperfusion injury, AMPK, cyclooxygenase-2, prostaglandin E2, myocardial infarct size, cardiomyocyte apoptosis, TNF-α, cardiac remodeling, obesity, cardioprotection
- MeSH terms
- Animals, Cells, Cultured, Mice, Inbred C57BL, Multienzyme Complexes, Nitrobenzenes, Sulfonamides, Tumor Necrosis Factor-alpha, Signal Transduction, Myocardial Reperfusion Injury, Cyclooxygenase Inhibitors, Myocardial Ischemia, Apoptosis, Protein Serine-Threonine Kinases, Mice, Knockout, Cytoprotection, Muscle Cells, Mice, Rats, Cyclooxygenase 2, Adiponectin, AMP-Activated Protein Kinases
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