ReviewSignal transduction and targeted therapy2026
Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.
Review in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Octopus-inspired suction-cup microneedle patch enables intralesional SMAD7/Budesonide co-delivery to disrupt TGF-β-driven fibrotic remodeling.Materials today. Bio · 2026Article
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- From Single Agents to Synergy: Redefining Therapeutic Strategies in MASLD.International journal of molecular sciences · 2026Review
- Ferroptosis-Inflammation Crosstalk: Mechanistic Insights and Emerging Drug Targets.Cell biochemistry and biophysics · 2026Review
- Effects of Water-Soluble CMolecules (Basel, Switzerland) · 2026Article
- Reparative "exosome-ark" for mitochondrial transplantation to reprogram macrophages and disrupt pathogenic crosstalk in pulmonary fibrosis.Materials today. Bio · 2026Article
- Multimodal Magnetic Resonance Imaging in Diabetic Kidney Disease: From Pathophysiological Insights to Clinical Applications.Diagnostics (Basel, Switzerland) · 2026Review
- Adenosine Signaling as a Central Integrative Network in Cellular Stress Responses and a Therapeutically Actionable Target in Human Disease.Biomolecules · 2026Review
- Pilot Study on the Use of Rheology and Low Field Nmr to Characterize the Liver of Obese Patients Undergoing Metabolic and Bariatric Surgery.International journal of molecular sciences · 2026Article
- Nintedanib Enhances the Antibacterial Activity of Bedaquiline Against Non-Tuberculous Mycobacteria: In vitro and in Mice Models.Infection and drug resistance · 2026Article
- Multifaceted mechanisms of unconventional T cells in ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Soft tissue mechanosensing and remodeling: the core regulatory role of Piezo/TRPV4 ion channels.Frontiers in cell and developmental biology · 2026Review
- Molecular insights of a Unani formulation in targeting fibrosis-associated diseases.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Fibrosis is a maladaptive pathophysiological process characterized by excessive deposition of extracellular matrix resulting from dysregulated tissue repair responses. Fibrosis can affect nearly all organ systems, such as the lung, heart, liver, and kidney. Persistent fibrotic remodeling leads to architectural distortion, loss of function, organ failure, and ultimately increased mortality. These devastating outcomes highlight the urgent need for effective antifibrotic therapies. Advances in multiomics technologies have revealed that fibrosis represents a dynamic alteration spanning the molecular, cellular, microenvironmental, and organ levels. Despite impressive progress in our understanding of fibrogenesis over recent years, a substantial translational gap remains between identifying potential antifibrotic targets and translating this theoretical knowledge into effective human therapies. To further understand pathogenesis and facilitate the development of novel antifibrotic drugs, this review summarizes crucial milestones in fibrosis research, elaborates on organ-specific pathogenic mechanisms, and details the phenotypic and functional changes in critical cellular players, including parenchymal cells, fibroblasts, endothelial cells, and immune cells. Furthermore, this review outlines the key signaling pathways implicated in the pathogenesis of fibrosis, provides a comprehensive overview of relevant clinical trials, and discusses promising future research directions, including cross-organ multiomics integration, chimeric antigen receptor therapy, and artificial intelligence technology applications.
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.