ReviewNature reviews. Drug discovery2025
Fibrosis: cross-organ biology and pathways to development of innovative drugs.
Review in Nature reviews. Drug discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 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
41 citing papers in PubMed.
- TGFβ-1 induces the release of BAG3 protein by human fibroblasts.Journal of translational medicine · 2026Article
- Fibrosis as the Engine of Kidney Functional Decline: Donald W. Seldin Young Investigator Award Lecture.Journal of the American Society of Nephrology : JASN · 2026Review
- Telomere-associated non-malignant pulmonary diseases: Pathogenic mechanisms and therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Next-generation molecular imaging of cardiac fibrosis.The international journal of cardiovascular imaging · 2026Review
- Shared mechanisms of organ fibrosis.JCI insight · 2026Review
- Unleashing innovative cross-organ fibrosis therapies by harnessing the omics revolution.JCI insight · 2026Review
- Fibroblasts: a diverse population of cells balancing homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer across organs.JCI insight · 2026Review
- Kat5 deficiency in alveolar type II cells licenses STAT6-driven glycolytic reprogramming and pulmonary fibrosis.Nature communications · 2026Article
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Aligned Fibronectin Microenvironment Temporally Facilitates Profibrotic Fibroblast Activation via Integrin α5β1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ZNF469 drives TGF-β1/SMAD3-mediated extracellular matrix regulation in pulmonary fibrosis.Biomolecules & biomedicine · 2026Article
- Prophylactic Effects of Combined Bosentan and Nintedanib on Early Post-Traumatic Joint Contracture Formation in a Rat Model.Journal of clinical medicine · 2026Article
- Deep phenotyping of skin tissue remodeling in patients with systemic sclerosis treated with CD19-CAR T cells.Nature communications · 2026Article
- Repressive chromatin regulates fibrotic potential through Suv39h1 in the heart.Cardiovascular research · 2026Article
- TNF-α and IL-1β but not IL-18 counteract TGF-β1 mediated stimulation of collagen accumulation and increased extracellular matrix strength and stiffness.Scientific reports · 2026Article
- Cellular and molecular regulation of fibrotic postoperative abdominal adhesions.American journal of physiology. Cell physiology · 2026Review
- Mechanisms of fibrotic tissue remodelling: insights from systemic sclerosis.Nature reviews. Rheumatology · 2026Review
- Valvular Leaflets Are Not Innocent Bystanders: Divergent Fibrotic Remodeling Accompanies Functional Mitral and Tricuspid Regurgitation.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Tissue-layer-resolved proteome landscape of Crohn's disease strictures highlights potential drivers of fibrosis progression.JCI insight · 2026Article
- Circadian Dysregulation in Aging Alters Senescence and Inflammatory Pathways in a Sex- and Time-of-Day-Dependent Manner.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
Abstract
Fibrosis is a pathophysiological mechanism involved in chronic and progressive diseases that results in excessive tissue scarring. Diseases associated with fibrosis include metabolic dysfunction-associated steatohepatitis (MASH), inflammatory bowel diseases (IBDs), chronic kidney disease (CKD), idiopathic pulmonary fibrosis (IPF) and systemic sclerosis (SSc), which are collectively responsible for substantial morbidity and mortality. Although a few drugs with direct antifibrotic activity are approved for pulmonary fibrosis and considerable progress has been made in the understanding of mechanisms of fibrosis, translation of this knowledge into effective therapies continues to be limited and challenging. With the aim of assisting developers of novel antifibrotic drugs, this Review integrates viewpoints of biologists and physician-scientists on core pathways involved in fibrosis across organs, as well as on specific characteristics and approaches to assess therapeutic interventions for fibrotic diseases of the lung, gut, kidney, skin and liver. This discussion is used as a basis to propose strategies to improve the translation of potential antifibrotic therapies.
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.