ArticleMolecular and cellular biochemistry2012
Hydrogen sulfide protects H9c2 cells against doxorubicin-induced cardiotoxicity through inhibition of endoplasmic reticulum stress.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 82 citations in OpenAlex.
- Proteomic Mechanisms of Hepatic- and Cardio-Protection of a Food-Hoarding Hibernator, Tamias sibiricus.Integrative zoology · 2026Article
- Endoplasmic Reticulum Stress in Acute Myeloid Leukemia: Pathogenesis, Prognostic Implications, and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Exploring SGLT2 Inhibitors' Activity in Breast Cancer: An Overview.Current topics in medicinal chemistry · 2025Review
- Sydnthiones are versatile bioorthogonal hydrogen sulfide donors.Nature communications · 2024Article
- Review
- Potential role of endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity-an update.Frontiers in pharmacology · 2024Review
- Dapagliflozin May Protect Against Doxorubicin-Induced Cardiotoxicity.Anatolian journal of cardiology · 2023Article
- Curcumin protects against doxorubicin induced oxidative stress by regulating the Keap1-Nrf2-ARE and autophagy signaling pathways.Psychopharmacology · 2023Article
- Hydropersulfides (RSSH) attenuate doxorubicin-induced cardiotoxicity while boosting its anticancer action.Redox biology · 2023Article
- HAntioxidants (Basel, Switzerland) · 2023Review
- NLRP3-mediated inflammation in cardio-oncology: sterile yet harmful.Translational research : the journal of laboratory and clinical medicine · 2023Review
- HFrontiers in chemistry · 2023Review
- Dapagliflozin protects against doxorubicin-induced cardiotoxicity by restoring STAT3.Archives of toxicology · 2022Article
- Spatiotemporal regulation of hydrogen sulfide signaling in the kidney.Redox biology · 2021Review
- Hydrogen sulfide improves ox‑LDL‑induced expression levels of Lp‑PLAMolecular medicine reports · 2021Article
- Dapagliflozin suppresses ER stress and protects doxorubicin-induced cardiotoxicity in breast cancer patients.Archives of toxicology · 2021Article
- Involvement of neurotrophic signaling in doxorubicin-induced cardiotoxicity.Experimental and therapeutic medicine · 2020Article
- Protective effect of bacterial lipase on lipopolysaccharide-induced toxicity in rat cardiomyocytes; H9C2 cell line.Journal of cardiovascular and thoracic research · 2020Article
- Protective effect of Shenmai injection on doxorubicin-induced cardiotoxicity via regulation of inflammatory mediators.BMC complementary and alternative medicine · 2019Article
- Supramolecular nanostructures with tunable donor loading for controlled HACS applied bio materials · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The roles of hydrogen sulfide (H(2)S) and endoplasmic reticulum (ER) stress in doxorubicin (DOX)-induced cardiotoxicity are still unclear. This study aimed to dissect the hypothesis that H(2)S could protect H9c2 cells against DOX-induced cardiotoxicity by inhibiting ER stress. Our results showed that exposure of H9c2 cells to DOX significantly inhibited the expression and activity of cystathionine-γ-lyase (CSE), a synthetase of H(2)S, accompanied by the decreased cell viability and the increased reactive oxygen species (ROS) accumulation. In addition, exposure of cells to H(2)O(2) (an exogenous ROS) mimicked the inhibitory effect of DOX on the expression and activity of CSE. Pretreatment with N-acetyl-L: -cysteine (NAC) (a ROS scavenger) attenuated intracellular ROS accumulation, cytotoxicity, and the inhibition of expression and activity of CSE induced by DOX. Notably, the ER stress-related proteins, including glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) were obviously upregulated in DOX-treated H9c2 cells. Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress. In conclusion, we have demonstrated that ROS-mediated inhibition of CSE is involved in DOX-induced cytotoxicity in H9c2 cells, and that exogenous H(2)S can confer protection against DOX-induced cardiotoxicity partly through inhibition of ER stress.
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