ReviewBritish journal of pharmacology2020
Redox à la carte: Novel chemogenetic models of heart failure.
Review in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Metabolomic and transcriptomic signatures of chemogenetic heart failure.American journal of physiology. Heart and circulatory physiology · 2022Article
- Chemogenetic Approaches to Probe Redox Pathways: Implications for Cardiovascular Pharmacology and Toxicology.Annual review of pharmacology and toxicology · 2022Article
- Complexities of the chemogenetic toolkit: Differential mDAAO activation by d-amino substrates and subcellular targeting.Free radical biology & medicine · 2021Article
- Redox à la carte: Novel chemogenetic models of heart failure.British journal of pharmacology · 2020Review
- Toward the Effective Bioengineering of a Pathological Tissue for Cardiovascular Disease Modeling: Old Strategies and New Frontiers for Prevention, Diagnosis, and Therapy.Frontiers in cardiovascular medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Many current animal models of heart failure are hampered by intrinsic methodological complexities, while other models yield only a subtle cardiac phenotype even after prolonged in vivo treatments. A new 'chemogenetic' animal model of heart failure reproduces a critical characteristic shared by many disease states that lead to heart failure in humans: an increase in redox stress in the heart. This 'chemogenetic' approach exploits a recombinant yeast enzyme that can be dynamically and specifically activated in vivo to generate the ROS hydrogen peroxide (H
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.