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Cited by 207

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Exercise Protects Against Myocardial Ischemia–Reperfusion Injury via Stimulation of β 3 -Adrenergic Receptors and Increased Nitric Oxide Signaling: Role of Nitrite and Nitrosothiols

Open access
Calvert, John W., Condit, Marah E., Aragón, Juan Pablo, Nicholson, Chad K., Moody, Bridgette F., Hood, Rebecca L., Sindler, Amy L., Gundewar, Susheel, Seals, Douglas R., Barouch, Lili A., Lefer, David J.·2011·Circulation Research

Abstract

Rationale: Exercise training confers sustainable protection against ischemia–reperfusion injury in animal models and has been associated with improved survival following a heart attack in humans. It is still unclear how exercise protects the heart, but it is apparent that endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) play a role. Objective: To determine the role of β 3 -adrenergic receptors (β 3 -ARs), eNOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of exercise. Methods and Results: Here we show that voluntary exercise reduces myocardial injury in mice following a 4-week training period and that these protective effects can be sustained for at least 1 week following the cessation of the training. The sustained cardioprotective effects of exercise are mediated by alterations in the phosphorylation status of eNOS (increase in serine 1177 and decrease in threonine 495), leading to an increase in NO generation and storage of NO metabolites (nitrite and nitrosothiols) in the heart. Further evidence revealed that the alterations in eNOS phosphorylation status and NO generation were mediated by β 3 -AR stimulation and that in response to exercise a deficiency of β 3 -ARs leads to an exacerbation of myocardial infarction following ischemia–reperfusion injury. Conclusions: Our findings clearly demonstrate that exercise protects the heart against myocardial ischemia–reperfusion injury by stimulation of β 3 -ARs and increased cardiac storage of nitric oxide metabolites (ie, nitrite and nitrosothiols).

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Crossref · 10.1161/circresaha.111.241117

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Metadata

Authors
Calvert, J. W., Condit, M. E., Aragón, J. P., Nicholson, C. K., Moody, B. F., Hood, R. L., Sindler, A. L., Gundewar, S., Seals, D. R., Barouch, L. A., & Lefer, D. J.
Venue
Circulation Research
Published
2011-06-10
Volume
108
Issue
12
Pages
1448-1458
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2107554716
Cited by
207
References
7
FWCI
9.60
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Exercise Protects Against Myocardial Ischemia–Reperfusion Injury via Stimulation of β 3 -Adrenergic Receptors and Increased Nitric Oxide Signaling: Role of Nitrite and Nitrosothiols. https://app.cochat.ai/papers/10.1161/circresaha.111.241117
The paper
Calvert, J. W., Condit, M. E., Aragón, J. P., Nicholson, C. K., Moody, B. F., Hood, R. L., Sindler, A. L., Gundewar, S., Seals, D. R., Barouch, L. A., & Lefer, D. J. (2011). Exercise Protects Against Myocardial Ischemia–Reperfusion Injury via Stimulation of β 3 -Adrenergic Receptors and Increased Nitric Oxide Signaling: Role of Nitrite and Nitrosothiols. Circulation Research. https://doi.org/10.1161/circresaha.111.241117

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.