ReviewAmerican journal of cardiovascular drugs : drugs, devices, and other interventions2022
The sGC-cGMP Signaling Pathway as a Potential Therapeutic Target in Doxorubicin-Induced Heart Failure: A Narrative Review.
Review in American journal of cardiovascular drugs : drugs, devices, and other interventions, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.
- Vericiguat in patients with heart failure across the spectrum of left ventricular ejection fraction: a patient-level, pooled meta-analysis of VITALITY-HFpEF and VICTORIA.Frontiers in endocrinology · 2024Pooled it
- Comparison of the Efficacy and Safety of Non-vitamin K Antagonist Oral Anticoagulants with Warfarin in Atrial Fibrillation Patients with a History of Bleeding: A Systematic Review and Meta-Analysis.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022Pooled it
- Therapeutic effect of Fuzheng Yixin decoction on cardiac insufficiencythe soluble guanylyl cyclase-cyclic guanosine monophosphate-protein kinase G pathway in a doxorubicin-induced dilated cardiomyopathy rat model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Chemokine-Guided Biomimetic Mn/Ce Nanozymes for Immunomodulation and Cardioprotection in Doxorubicin-Induced Cardiomyopathy.Advanced healthcare materials · 2026Article
- Cardioprotective Effects of Soluble Guanylate Cyclase and Its α1 Subunit on Myocardial Ischemia/Reperfusion Injury via the PGC-1α/UCP2 Pathway.Journal of cardiovascular pharmacology · 2026Article
- Pathological mechanisms and clinical research progress of endothelial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Vericiguat improves cardiac remodelling and function in rats with doxorubicin-induced cardiomyopathy.ESC heart failure · 2025Article
- Characterization of a new model of chemotherapy-induced heart failure with reduced ejection fraction and nephrotic syndrome in Ren-2 transgenic rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Sophocarpine alleviates doxorubicin-induced heart injury by suppressing oxidative stress and apoptosis.Scientific reports · 2024Article
- Epigenetic Signatures in Arterial Hypertension: Focus on the Microvasculature.International journal of molecular sciences · 2023Review
- Calcium Overload or Underload? The Effects of Doxorubicin on the Calcium Dynamics in Guinea Pig Hearts.Biomedicines · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The anti-cancer agent doxorubicin (DOX) has high cardiotoxicity that is linked to DOX-mediated increase in oxidative stress, mitochondrial iron overload, DNA damage, autophagy, necrosis, and apoptosis, all of which are also associated with secondary tumorigenicity. This limits the clinical application of DOX therapies. Previous studies have attributed DOX-mediated cardiotoxicity to mitochondrial iron accumulation and the production of reactive oxygen species (ROS), which seem to be independent of its anti-tumor DNA damaging effects. Chemo-sensitization of soluble guanylate cyclase (sGC) in the cyclic guanosine monophosphate (cGMP) pathway induces tumor cell death despite the cardiotoxicity associated with DOX treatment. However, sGC-cGMP signaling must be activated during heart failure to facilitate myocardial cell survival. The sGC pathway is dependent on nitric oxide and signal transduction via the nitric oxide-sGC-cGMP pathway and is attenuated in various cardiovascular diseases. Additionally, cGMP signaling is regulated by the action of certain phosphodiesterases (PDEs) that protect the heart by inhibiting PDE, an enzyme that hydrolyses cGMP to GMP activity. In this review, we discuss the studies describing the interactions between cGMP regulation and DOX-mediated cardiotoxicity and their application in improving DOX therapeutic outcomes. The results provide novel avenues for the reduction of DOX-induced secondary tumorigenicity and improve cellular autonomy during DOX-mediated cardiotoxicity.
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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.