ReviewChemical communications (Cambridge, England)2022
Myofibroblast specific targeting approaches to improve fibrosis treatment.
Review in Chemical communications (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Systematic review of extracellular vesicle-derived microRNAs involved in organ fibrosis: implications for arthrofibrosis therapy.Journal of translational medicine · 2025Pooled it
- Is there a link between fascia and cancer? From potential mechanisms to future treatment options.Frontiers in physiology · 2026Review
- Beyond Organ-Specific Therapies: A Unified Approach to Multi-Organ Fibrosis.Drug design, development and therapy · 2026Review
- Epac1 Inhibits Orbital Fibroblast Activation to Ameliorate Thyroid-Associated Orbitopathy-Like Features Through the JAK/STAT Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
- The mechanotransduction-immune axis in organ fibrosis: dual regulatory mechanisms and translational therapeutic perspectives.Frontiers in immunology · 2025Review
- BRD4: an effective target for organ fibrosis.Biomarker research · 2024Review
- Characterization of patient-derived intestinal organoids for modelling fibrosis in Inflammatory Bowel Disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Zinc-alpha-2-glycoprotein Secreted by Triple-Negative Breast Cancer Promotes Peritumoral Fibrosis.Cancer research communications · 2024Article
- Modelling and targeting mechanical forces in organ fibrosis.Nature reviews bioengineering · 2024Article
- Article
- Emerging delivery approaches for targeted pulmonary fibrosis treatment.Advanced drug delivery reviews · 2024Review
- Progress and prospect of nanotechnology for cardiac fibrosis treatment.Interdisciplinary medicine · 2023Review
- Insulin-Like Growth Factor 1 Receptor Deficiency Alleviates Angiotensin II-Induced Cardiac Fibrosis Through the Protein Kinase B/Extracellular Signal-Regulated Kinase/Nuclear Factor-κB Pathway.Journal of the American Heart Association · 2023Article
- A photothermal driven chemotherapy for the treatment of metastatic melanoma.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Underlying Molecular Mechanism and Construction of a miRNA-Gene Network in Idiopathic Pulmonary Fibrosis by Bioinformatics.International journal of molecular sciences · 2023Article
- Potential and Progress of 2D Materials in Photomedicine for Cancer Treatment.ACS applied bio materials · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Fibrosis has been shown to develop in individuals with underlying health conditions, especially chronic inflammatory diseases. Fibrosis is often diagnosed in various organs, including the liver, lungs, kidneys, heart, and skin, and has been described as excessive accumulation of extracellular matrix that can affect specific organs in the body or systemically throughout the body. Fibrosis as a chronic condition can result in organ failure and result in death of the individual. Understanding and identification of specific biomarkers associated with fibrosis has emerging potential in the development of diagnosis and targeting treatment modalities. Therefore, in this review, we will discuss multiple signaling pathways such as TGF-β, collagen, angiotensin, and cadherin and outline the chemical nature of the different signaling pathways involved in fibrogenesis as well as the mechanisms. Although it has been well established that TGF-β is the main catalyst initiating and driving multiple pathways for fibrosis, targeting TGF-β can be challenging as this molecule regulates essential functions throughout the body that help to keep the body in homeostasis. We also discuss collagen, angiotensin, and cadherins and their role in fibrosis. We comprehensively discuss the various delivery systems used to target collagen, angiotensin, and cadherins to manage fibrosis. Nevertheless, understanding the steps by which this molecule drives fibrosis development can aid in the development of specific targets of its cascading mechanism. Throughout the review, we will demonstrate the mechanism of fibrosis targeting to improve targeting delivery and therapy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.