ArticleHeart and vessels2012
Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury.
Article in Heart and vessels, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Graphene Oxide Enhances Biogenesis and Release of Exosomes in Human Ovarian Cancer Cells.International journal of nanomedicine · 2022Article
- Endogenous SOFrontiers in cell and developmental biology · 2021Review
- Catalase as a sulfide-sulfur oxido-reductase: An ancient (and modern?) regulator of reactive sulfur species (RSS).Redox biology · 2017Article
- Endogenous Sulfur Dioxide Inhibits Vascular Calcification in Association with the TGF-β/Smad Signaling Pathway.International journal of molecular sciences · 2016Article
- Endogenous Sulfur Dioxide: A New Member of Gasotransmitter Family in the Cardiovascular System.Oxidative medicine and cellular longevity · 2016Review
- LipoxinA4 attenuates myocardial ischemia reperfusion injury via a mechanism related to downregulation of GRP-78 and caspase-12 in rats.Heart and vessels · 2014Article
- The role of sulfur dioxide in the regulation of mitochondrion-related cardiomyocyte apoptosis in rats with isopropylarterenol-induced myocardial injury.International journal of molecular sciences · 2013Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been demonstrated that excessively activated endoplasmic reticulum stress (ERS) is related to myocardial injury. The study was designed to explore the possible role of sulfur dioxide (SO(2)) in protecting excessively activated ERS in rats with isoproterenol (ISO)-induced myocardial injury. Wistar rats were randomly divided into control, ISO, and ISO + SO(2) groups. Cardiac catheterization-derived hemodynamic parameters and myocardial enzymes in plasma were measured. Microstructure changes in myocardial tissues were examined. Cardiomyocyte apoptosis was detected by TUNEL method. Myocardial SO(2) content and aspartate amino transferase (AAT) activity were detected. Meanwhile, protein and mRNA expressions of myocardial AAT1, AAT2, and ERS markers (GRP78, caspase-12, and CHOP) were evaluated. The results showed that cardiac function was decreased, myocardial microstructure was damaged, and myocardial enzyme levels and cardiomyocyte apoptosis were increased with a downregulated endogenous AAT/SO(2) pathway, and that ERS markers were upregulated at transcriptional and translational levels in ISO-treated rats. However, the administration of an SO(2) donor, resulting in an increased SO(2) content in myocardial tissues, improved cardiac function and myocardial structure, and ameliorated myocardial enzyme levels and cardiomyocyte apoptosis associated with a downregulation of excessively activated ERS. In conclusion, the endogenous AAT/SO(2) pathway was probably responsible for the inhibition of excessively activated ERS, which might be involved in the mechanism of ISO-induced myocardial injury.
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