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Cited by 316

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Acute exercise stress activates Nrf2/ARE signaling and promotes antioxidant mechanisms in the myocardium

Open access
Muthusamy, Vasanthi R., Kannan, Sankaranarayanan, Sadhaasivam, Kamal, Gounder, Sellamuthu S., Davidson, Christopher J., Boeheme, Christoph, Hoidal, John R., Wang, Li, Rajasekaran, Namakkal Soorappan·2012·Free Radical Biology and Medicine
DOI 10.1016/j.freeradbiomed.2011.10.440
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Abstract

Oxidative stress has been implicated in the pathogenesis of cardiovascular diseases, including myocardial hypertrophy and infarction. Although impairment of antioxidant defense mechanisms has been thought to provoke oxidative stress-induced myocardial dysfunction, it has been difficult to clearly demonstrate. Nuclear erythroid 2 p45-related factor 2 (Nrf2) is a redox-sensitive, basic leucine zipper protein that regulates the transcription of several antioxidant genes. We previously reported that sustained activation of Nrf2 upregulates transcription of a number of endogenous antioxidants in the heart. Here, we show that acute exercise stress (AES) results in activation of Nrf2/ARE (antioxidant response element) signaling and subsequent enhancement of antioxidant defense pathways in wild-type (WT) mouse hearts, while oxidative stress, along with blunted defense mechanisms, was observed in Nrf2−/− mice. We also find that AES is associated with increased trans-activation of ARE-containing genes in exercised animals when compared to age-matched sedentary WT mice. However, enhanced oxidative stress in response to AES was observed in Nrf2−/− mice due to lower basal expression and marked attenuation of the transcriptional induction of several antioxidant genes. Thus, AES induces ROS and promotes Nrf2 function, but disruption of Nrf2 increases susceptibility of the myocardium to oxidative stress. Our findings suggest the basis for a nonpharmacological approach to activate Nrf2/ARE signaling, which might be a potential therapeutic target to protect the heart from oxidative stress-induced cardiovascular complications.

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Metadata

Authors
Muthusamy, V. R., Kannan, S., Sadhaasivam, K., Gounder, S. S., Davidson, C. J., Boeheme, C., Hoidal, J. R., Wang, L., & Rajasekaran, N. S.
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2012-01
Volume
52
Issue
2
Pages
366-376
ISSN
0891-5849 (ISSN-L)
DOI
10.1016/j.freeradbiomed.2011.10.440
OpenAlex
W2044560810
Cited by
316
References
11
FWCI
5.41
Type
journal article
Language
en
Open access
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CoChat. (2026). Citation check: Acute exercise stress activates Nrf2/ARE signaling and promotes antioxidant mechanisms in the myocardium. https://app.cochat.ai/papers/10.1016/j.freeradbiomed.2011.10.440
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Muthusamy, V. R., Kannan, S., Sadhaasivam, K., Gounder, S. S., Davidson, C. J., Boeheme, C., Hoidal, J. R., Wang, L., & Rajasekaran, N. S. (2012). Acute exercise stress activates Nrf2/ARE signaling and promotes antioxidant mechanisms in the myocardium. Free Radical Biology and Medicine. https://doi.org/10.1016/j.freeradbiomed.2011.10.440

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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.