ReviewInternational journal of molecular sciences2022
Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- A first-in-human phase I study of SHR-1906, a humanized monoclonal antibody against connective tissue growth factor, in healthy participants.Clinical and translational science · 2023Trial
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- Krüppel-like factor 14 enhances fatty acid oxidation to combat pulmonary fibrosis.Respiratory research · 2026Article
- The CaInternational journal of molecular sciences · 2026Article
- Freezing shock monocytes deliver antisense oligonucleotides via liposomes for the treatment of idiopathic pulmonary fibrosis.Asian journal of pharmaceutical sciences · 2026Article
- TGF-β: The Molecular Mechanisms of Atherosclerosis - insights into SMAD Pathways and Gene Therapy Prospects.Current medicinal chemistry · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Recent understanding of immunometabolic remodeling in pulmonary macrophages: homeostasis, chronic respiratory diseases, and therapeutic targeting.Frontiers in pharmacology · 2026Review
- S1PR3 Inhibition in alveolar epithelial cells alleviates pulmonary fibrosis by enhancing alveolar barrier function.Respiratory research · 2025Article
- Mechanosensitive genomic enhancers potentiate the cellular response to matrix stiffness.Science (New York, N.Y.) · 2025Article
- Bidirectional Interaction Between PGEProteomes · 2025Article
- Role of macrophage ATP metabolism disorder in SiOPurinergic signalling · 2025Review
- Article
- Interactions of flavonoid and coumarin derivative compounds with transforming growth factor-beta receptor 1 (TGF-βR1): integrating virtual screening, molecular dynamics, maximum common substructure, and ADMET approaches in the treatment of idiopathic pulmonary fibrosis.Journal of molecular modeling · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- CCN2 mediates fibroblast-macrophage interaction in knee arthrofibrosis based on single-cell RNA-seq analysis.Bone research · 2025Article
- Yap Is a Nutrient Sensor Sensitive to the Amino Acid L-Isoleucine and Regulates the Expression of Ctgf in Cardiomyocytes.Biomolecules · 2024Article
- Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024Review
- Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart.Circulation research · 2024Article
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had been identified in different IPF lung cells (alveolar epithelial cells, alveolar endothelial cells, fibroblasts, and macrophages). Here, we reviewed the role of the CTGF in IPF lung cells to mediate anomalous senescence-related metabolic mechanisms that support the fibrotic environment in IPF.
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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.