ReviewNaunyn-Schmiedeberg's archives of pharmacology2021
Inflammation suppression in doxorubicin-induced cardiotoxicity: natural compounds as therapeutic options.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Sotagliflozin ameliorates doxorubicin-induced cardiomyopathy by regulating inflammation and mitochondrial dysfunction through the AMPK/mTOR pathway.Experimental and therapeutic medicine · 2026Article
- P2Y12-AMPKα2 signaling contributes to cardiomyocyte senescence in doxorubicin-induced heart failure.Molecular and cellular biochemistry · 2026Article
- Biochanin A attenuates doxorubicin-induced cardiotoxicity in rats with associated modulation of PI3K/Akt/mTOR and p38 MAPK signaling.Frontiers in cardiovascular medicine · 2026Article
- Article
- Pleiotropic role of CCR9/CCL25 signaling in adriamycin-induced cardiomyopathy.Journal of advanced research · 2025Article
- Targeting the NLRP3 by Natural Compounds: Therapeutic Strategies to Mitigate Doxorubicin-Induced Cardiotoxicity.Cell biochemistry and biophysics · 2025Review
- Review
- Review
- Network analysis and experimental validation to investigateFrontiers in pharmacology · 2025Article
- CTRP5 Attenuates Doxorubicin-Induced Cardiotoxicity Via Inhibiting TLR4/NLRP3 Signaling.Cardiovascular drugs and therapy · 2024Article
- Molecular mechanisms involved in therapeutic effects of natural compounds against cisplatin-induced cardiotoxicity: a review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- PARP-2 mediates cardiomyocyte aging and damage induced by doxorubicin through SIRT1 Inhibition.Apoptosis : an international journal on programmed cell death · 2024Article
- Role of gut microbiota in doxorubicin-induced cardiotoxicity: from pathogenesis to related interventions.Journal of translational medicine · 2024Review
- Molecular mechanisms involved in doxorubicin-induced cardiotoxicity: A bibliometrics analysis by VOSviewer.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Noninvasive neuromodulation protects against doxorubicin-induced cardiotoxicity and inhibits tumor growth.iScience · 2024Article
- DL-3-Heliyon · 2024Article
- The Role of mTOR in Doxorubicin-Altered Cardiac Metabolism: A Promising Therapeutic Target of Natural Compounds.Cardiovascular toxicology · 2024Review
- Pharmacological properties of Polygonatum and its active ingredients for the prevention and treatment of cardiovascular diseases.Chinese medicine · 2024Review
- Nrf2: a dark horse in doxorubicin-induced cardiotoxicity.Cell death discovery · 2023Review
- Boesenbergia rotunda displayed anti-inflammatory, antioxidant and anti-apoptotic efficacy in doxorubicin-induced cardiotoxicity in rats.Scientific reports · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is a potent chemotherapeutic agent; however, the accompanying cardiotoxicity is a significant complication of the usefulness of treatment with DOX. Multiple mechanisms have been suggested for this often fatal side effect, one of which is inflammation. Several pathways with different targets have been reported to result in DOX-induced heart inflammation. Some natural occurring compounds (NCs) have been reported to interact with the DOX-induced cardiotoxicity through targeting one or more of several pathways, including the Nrf2/NF-kB, TLR-4/NF-kB, MAPK/NF-kB, and NLRP3 inflammasome pathways. This article reviews several of these pathways and the potential protective effect of some NCs against the cardiac inflammation induced by DOX.
Indexed as
Identifiers
What OpenQuestion holds
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.