ArticleScientific reports2017
Complement 5a Receptor deficiency does not influence adverse cardiac remodeling after pressure-overload in mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 12 citations in OpenAlex.
- Absence of GDF15 Aggravates Pressure Overload-Induced Cardiac Remodelling in Mice Hallmarked by Perivascular Fibrosis and Signs of Endothelial-to-Mesenchymal Transition.International journal of molecular sciences · 2026Article
- Genetic and metabolomic pathways linking frailty, chronic kidney disease, and kidney failure: a Mendelian randomization and multi-omics analysis.Renal failure · 2025Article
- Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway.Pharmaceutical biology · 2022Article
- Characterization of early myocardial inflammation in ischemia-reperfusion injury.Frontiers in immunology · 2022Article
- Mildly Increased Renin Expression in the Absence of Kidney Injury in the Murine Transverse Aortic Constriction Model.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertension is one of the most common risk factors for the development heart failure in the general population. Inflammation plays a central role in this adverse remodeling and eventually to the development of heart failure. Circulating levels of Complement factor 5a (C5a) are increased in hypertensive patients and the C5a receptor is associated with the presence of cardiac fibrosis and inflammation in an experimental hypertension model. To test if C5aR is involved in adverse cardiac remodeling following pressure-overload, we induced transverse aortic constriction (TAC) in wildtype and C5a receptor deficient mice (C5aR
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