ReviewMatrix biology : journal of the International Society for Matrix Biology2020
Targeting the renin-angiotensin-aldosterone system in fibrosis.
Review in Matrix biology : journal of the International Society for Matrix Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 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
118 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.
- Mesenteric Fibrosis in Neuroendocrine Neoplasms: a Systematic Review of New Thoughts on Causation and Potential Treatments.Current oncology reports · 2025Pooled it
- Multifunctional biomaterial platforms for blocking the fibrosis process and promoting cellular restoring effects in myocardial fibrosis therapy.Frontiers in bioengineering and biotechnology · 2022Pooled it
- Effect of anti-fibrotic therapy on regression of myocardial fibrosis after TAVI: design and rationale of the Reduce-MFA DZHK25 trial.ESC heart failure · 2026Trial
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Article
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Mass spectrometry-based urinary proteomic analysis in feline chronic kidney disease.Physiological reports · 2026Article
- Mineralocorticoid Receptor Antagonists for Liver Fibrosis: Potential Mechanisms and Research Progress.Journal of clinical and translational hepatology · 2026Review
- Decoding cardiorenal crosstalk: Intercellular communication mechanisms and therapeutic insights in cardiorenal syndrome.iScience · 2026Review
- Association between particulate matter air pollution and subclinical myocardial fibrosis in structurally normal hearts: a CMR-based study.European heart journal. Cardiovascular Imaging · 2026Article
- PLIN5 Protects Against Ang II-Induced Podocyte Lipotoxicity by Interacting With FKBP8 and Preserving Lipid Droplet-Mitochondria Contact.Cell proliferation · 2026Article
- Butyrate and Butyrate-Producing Bacteria in Cardiovascular-Kidney-Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2026Review
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Applying dendrimer nanoprobes to the diagnosis and evaluation of kidney fibrosis.Nanomedicine (London, England) · 2026Review
- Lipids in kidney diseases: from systemic imbalance to intrarenal alterations of cellular lipid metabolism in rare and common kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2026Review
- PRIP/PLCL deficiency activates PI3K-AKT-YAP signaling and promotes organ fibrosis.Cell communication and signaling : CCS · 2026Article
- Beyond Organ-Specific Therapies: A Unified Approach to Multi-Organ Fibrosis.Drug design, development and therapy · 2026Review
- Beyond blood pressure: the renin-angiotensin system as an innovative driver and therapeutic target in pathological scarring.Frontiers in pharmacology · 2026Review
- Chronic Rejection in Facial Vascularized Composite Allotransplantation (fVCA).Results and problems in cell differentiation · 2026Review
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Fibrosis is characterized by excessive deposition of extracellular matrix components such as collagen in tissues or organs. Fibrosis can develop in the heart, kidneys, liver, skin or any other body organ in response to injury or maladaptive reparative processes, reducing overall function and leading eventually to organ failure. A variety of cellular and molecular signaling mechanisms are involved in the pathogenesis of fibrosis. The renin-angiotensin-aldosterone system (RAAS) interacts with the potent Transforming Growth Factor β (TGFβ) pro-fibrotic pathway to mediate fibrosis in many cell and tissue types. RAAS consists of both classical and alternative pathways, which act to potentiate or antagonize fibrotic signaling mechanisms, respectively. This review provides an overview of recent literature describing the roles of RAAS in the pathogenesis of fibrosis, particularly in the liver, heart, kidney and skin, and with a focus on RAAS interactions with TGFβ signaling. Targeting RAAS to combat fibrosis represents a promising therapeutic approach, particularly given the lack of strategies for treating fibrosis as its own entity, thus animal and clinical studies to examine the impact of natural and synthetic substances to alter RAAS signaling as a means to treat fibrosis are reviewed as well.
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.