ReviewFrontiers in cardiovascular medicine2022
The Scientific Rationale for the Introduction of Renalase in the Concept of Cardiac Fibrosis.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Renalase stimulates aldosterone production via PMCA4b/cAMP in NCI-H295R cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Systemic Molecular Alterations ofInternational journal of molecular sciences · 2026Article
- Sirtuins as Endogenous Regulators of Cardiac Fibrosis: A Current Perspective.Cardiovascular toxicology · 2025Review
- Single-cell RNA sequencing reveals the potential role of Postn(+) fibroblasts in promoting the progression of myocardial fibrosis after myocardial infarction.Scientific reports · 2025Article
- The Multi-Faceted Nature of Renalase for Mitochondrial Dysfunction Improvement in Cardiac Disease.Cells · 2023Review
- Cardiac-specific renalase overexpression alleviates CKD-induced pathological cardiac remodeling in mice.Frontiers in cardiovascular medicine · 2022Article
- Renalase Challenges the Oxidative Stress and Fibroproliferative Response in COVID-19.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis represents a redundant accumulation of extracellular matrix proteins, resulting from a cascade of pathophysiological events involved in an ineffective healing response, that eventually leads to heart failure. The pathophysiology of cardiac fibrosis involves various cellular effectors (neutrophils, macrophages, cardiomyocytes, fibroblasts), up-regulation of profibrotic mediators (cytokines, chemokines, and growth factors), and processes where epithelial and endothelial cells undergo mesenchymal transition. Activated fibroblasts and myofibroblasts are the central cellular effectors in cardiac fibrosis, serving as the main source of matrix proteins. The most effective anti-fibrotic strategy will have to incorporate the specific targeting of the diverse cells, pathways, and their cross-talk in the pathogenesis of cardiac fibroproliferation. Additionally, renalase, a novel protein secreted by the kidneys, is identified. Evidence demonstrates its cytoprotective properties, establishing it as a survival element in various organ injuries (heart, kidney, liver, intestines), and as a significant anti-fibrotic factor, owing to its,
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