ReviewFrontiers in medicine2025
The role of the classical renin-angiotensin system and angiotensin-converting enzyme 2/Ang(1-7)/Mas axis in pulmonary fibrosis.
Review in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Axial Connectivity of the Lung Microbiome: A Review of Interorgan Crosstalk.Comprehensive physiology · 2026Review
- Beyond the Heart-Lung Axis: A Review of the Crosstalk Between the Hemodynamic, Neurohormonal, and Immune Systems in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- The Heart-Kidney Axis in Heart Failure and Chronic Kidney Disease: Mechanisms, Mediators, and Therapeutic Implications.Biomolecules · 2026Review
- Article
- The Isolation and Characterization of ACE Inhibitory Peptides fromFoods (Basel, Switzerland) · 2026Article
- Pathogen-Specific Regulation of Renin-Angiotensin System Genes in Epithelial Cells: A Comparative Study of SARS-CoV-2 Spike Protein N-Terminal Domain Fragment and Bacterial Lipopolysaccharide.Pathogens (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis (PF), a progressive and fatal disease, is characterized by fibroblast proliferation, excessive extracellular matrix deposition, and collagen synthesis. These pathological changes lead to impaired lung structure and function, ultimately resulting in respiratory failure. Emerging basic and clinical evidence highlight the renin-angiotensin system (RAS) as a critical contributor to PF onset and progression. Angiotensin (Ang) II, a key RAS component, mediates various biological effects through its receptors, Ang II receptor type 1 (AT
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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.