ArticleMolecular and cellular biochemistry2018
Histamine 2 receptor antagonism elicits protection against doxorubicin-induced cardiotoxicity in rodent model.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Iron homeostasis and ferroptosis in muscle diseases and disorders: mechanisms and therapeutic prospects.Bone research · 2025Review
- Mechanistic Insights into Flavonoid Subclasses as Cardioprotective Agents Against Doxorubicin-Induced Cardiotoxicity: A Comprehensive Review.Drug design, development and therapy · 2025Review
- Inhibitors of gastric acid secretion increase oxidative stress and matrix metalloproteinase-2 activity leading to vascular remodeling.Molecular and cellular biochemistry · 2024Article
- Antacid Therapy in Coronary Artery Disease and Heart Failure: Proton Pump Inhibitors vs. HCardiovascular drugs and therapy · 2024Review
- Histamine receptors in heart failure.Heart failure reviews · 2022Review
- Paving the way for small-molecule drug discovery.American journal of translational research · 2021Review
- What is considered cardiotoxicity of anthracyclines in animal studies.Oncology reports · 2020Review
- Doxorubicin‑induced oxidative and nitrosative stress: Mitochondrial connexin 43 is at the crossroads.International journal of molecular medicine · 2020Article
- Accelerated cardiomyocyte senescence contributes to late-onset doxorubicin-induced cardiotoxicity.American journal of physiology. Cell physiology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX), an anthracycline-based antibiotic, is regularly used in the management of carcinomas, and haematological malignancies have been downplayed in chemotherapy because of its ability to induce dilated cardiomyopathy (DCM). Dexrazoxane is approved to combat the cardiotoxicity, but limited by its adverse effects. Redox imbalance and reactive oxygen species generation plays major role in DOX-induced cardiotoxicity. Histamine, known to mediate various cardiovascular effects, but nevertheless the role of histamine or its receptors in DOX-induced DCM is remained obscure. Hence, this study is aimed to examine the effect of Famotidine (FAM), a H2 receptor antagonist on DOX-induced DCM in Wistar rats. Myocardial antioxidant status, stress and apoptosis markers, myocardial morphology and function were evaluated as the end points. Treatment with FAM has alleviated DOX doxorubicin-induced cardiotoxicity by reducing oxidative and nitrosative stress evident from lipid peroxidation and total nitrate-to-nitrite ratio, and enhanced the activity of super oxide dismutase. Cardiac stress markers like LDH and Na
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Registered trials
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.