ArticleCardiovascular toxicology2013
Protection from oxidative and electrophilic stress in the Gsta4-null mouse heart.
Article in Cardiovascular toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Colonic expression of glutathioneHeliyon · 2023Article
- DNA methylation and mRNA expression of glutathione S-transferase alpha 4 are associated with intracranial aneurysms in a gender-dependent manner.Frontiers in genetics · 2022Article
- Proteomic Analysis of Cardiac Adaptation to Exercise by High Resolution Mass Spectrometry.Frontiers in molecular biosciences · 2021Article
- Protection against Doxorubicin-Related Cardiotoxicity by Jaceosidin Involves the Sirt1 Signaling Pathway.Oxidative medicine and cellular longevity · 2021Article
- Sulforaphane prevents age-associated cardiac and muscular dysfunction through Nrf2 signaling.Aging cell · 2020Article
- N-acetylcysteine targets 5 lipoxygenase-derived, toxic lipids and can synergize with prostaglandin EAnnals of neurology · 2018Article
- Role of the pregnane X receptor in binge ethanol-induced steatosis and hepatotoxicity.The Journal of pharmacology and experimental therapeutics · 2018Article
- Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model.PloS one · 2018Article
- Sulforaphane protects the heart from doxorubicin-induced toxicity.Free radical biology & medicine · 2015Article
- Effects of Local Heart Irradiation in a Glutathione S-Transferase Alpha 4-Null Mouse Model.Radiation research · 2015Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
4-Hydroxynonenal (4-HNE) mediates many pathological effects of oxidative and electrophilic stress and signals to activate cytoprotective gene expression regulated by NF-E2-related factor 2 (Nrf2). By exhibiting very high levels of 4-HNE-conjugating activity, the murine glutathione transferase alpha 4 (GSTA4-4) helps regulate cellular 4-HNE levels. To examine the role of 4-HNE in vivo, we disrupted the murine Gsta4 gene. Gsta4-null mice exhibited no cardiac phenotype under normal conditions and no difference in cardiac 4-HNE level as compared to wild-type mice. We hypothesized that the Nrf2 pathway might contribute an important compensatory mechanism to remove excess cardiac 4-HNE in Gsta4-null mice. Cardiac nuclear extracts from Gsta4-null mice exhibited significantly higher Nrf2 binding to antioxidant response elements. We also observed responses in critical Nrf2 target gene products: elevated Sod2, Cat, and Akr1b7 mRNA levels and significant increases in both cardiac antioxidant and anti-electrophile enzyme activities. Gsta4-null mice were less sensitive and maintained normal cardiac function following chronic doxorubicin treatment, known to increase cardiac 4-HNE levels. Hence, in the absence of GSTA4-4 to modulate both physiological and pathological 4-HNE levels, the adaptive Nrf2 pathway may be primed to contribute to a preconditioned cardiac phenotype in the Gsta4-null mouse.
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Registered trials
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