ArticleCell death & disease2016
Gp130-mediated STAT3 activation by S-propargyl-cysteine, an endogenous hydrogen sulfide initiator, prevents doxorubicin-induced cardiotoxicity.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- STAT-Mediated Mitochondrial Regulation in Cardiovascular Diseases: Mechanistic Insights and STAT3-Focused Therapeutic Strategies.Biomolecules · 2026Review
- Ring Finger Protein 2 Promotes Oxidative Stress and Mitochondrial Dysfunction in Doxorubicin-Induced Cardiotoxicity Via the Mercaptopyruvate Sulfurtransferase/Hydrogen Sulfide Pathway.Journal of the American Heart Association · 2025Article
- S-Propargyl-Cysteine Attenuates Stroke Heterogeneity via Promoting Protective Autophagy Across Multiple Neural Cell Types: Insights From Single-Cell Sequencing.CNS neuroscience & therapeutics · 2025Article
- HMGB1/TREM1 crosstalk between heat-injured hepatocytes and macrophages promotes HCC progression after RFA.Journal of cancer research and clinical oncology · 2024Article
- Bone morphogenetic protein 10 alleviates doxorubicin-induced cardiac injury via signal transducer and activator of transcription 3 signaling pathway.Bioengineered · 2022Article
- I-κB kinase-ε deficiency improves doxorubicin-induced dilated cardiomyopathy by inhibiting the NF-κB pathway.Frontiers in physiology · 2022Article
- HBiomolecules · 2021Review
- Regulation of STAT3 and its role in cardioprotection by conditioning: focus on non-genomic roles targeting mitochondrial function.Basic research in cardiology · 2021Review
- Tumour-derived substrate-adherent cells promote neuroblastoma survival through secreted trophic factors.Molecular oncology · 2021Article
- Article
- Molecular mechanisms of anthracycline cardiovascular toxicity.Clinical science (London, England : 1979) · 2021Review
- Trends in HAntioxidants (Basel, Switzerland) · 2021Review
- Hydrogen Sulfide: a Novel Immunoinflammatory Regulator in Rheumatoid Arthritis.Advances in experimental medicine and biology · 2021Review
- Vanillin Prevents Doxorubicin-Induced Apoptosis and Oxidative Stress in Rat H9c2 Cardiomyocytes.Nutrients · 2020Article
- Osteocrin attenuates inflammation, oxidative stress, apoptosis, and cardiac dysfunction in doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2020Article
- STAT3 for Cardiac Regenerative Medicine: Involvement in Stem Cell Biology, Pathophysiology, and Bioengineering.International journal of molecular sciences · 2020Review
- Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis.Oxidative medicine and cellular longevity · 2020Review
- An Appraisal of Developments in Allium Sulfur Chemistry: Expanding the Pharmacopeia of Garlic.Molecules (Basel, Switzerland) · 2019Review
- ZYZ-803 Mitigates Endoplasmic Reticulum Stress-Related Necroptosis after Acute Myocardial Infarction through Downregulating the RIP3-CaMKII Signaling Pathway.Oxidative medicine and cellular longevity · 2019Article
- An Update on the Multifaceted Roles of STAT3 in the Heart.Frontiers in cardiovascular medicine · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (Dox) could trigger a large amount of apoptotic cells in the myocardium, which leads to dilated cardiomyopathy and heart failure. S-propargyl-cysteine (SPRC), a producing agent of endogenous hydrogen sulfide (H2S), possesses cardioprotective efficacy. However, the specific effect and mechanism of SPRC in Dox-induced cardiotoxicity remain elusive. Given gp130 with its main downstream signaling molecule, signal transducer and activator of transcription 3 (STAT3), is involved in cardiac myocyte survival and growth; the present study was performed to elucidate whether SPRC counteracts Dox-induced cardiotoxicity, and if so, whether the gp130/STAT3 pathway is involved in this cardioprotective activity. SPRC stimulated the activation of STAT3 via gp130-mediated transduction tunnel in vitro and in vivo. In Dox-stimulated cardiotoxicity, SPRC enhanced cell viability, restored expression of gp130/STAT3-regulated downstream genes, inhibited apoptosis and oxidative stress, and antagonized mitochondrial dysfunction and intracellular Ca(2+) overload. Intriguingly, blockade of gp130/STAT3 signaling abrogated all these beneficial capacities of SPRC. Our findings present the first piece of evidence for the therapeutic properties of SPRC in alleviating Dox cardiotoxicity, which could be attributed to the activation of gp130-mediated STAT3 signaling. This will offer a novel molecular basis and therapeutic strategy of H2S donor for the treatment of heart failure.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.