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 54 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
54 citing papers in PubMed.
- Fibronectin's tensional state as a mechanical signature of fibrotic extracellular matrix in idiopathic pulmonary fibrosis models.Matrix biology plus · 2026Article
- Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026Review
- New approach methodologies: drug screening platform to identify antifibrotic compounds.Nature protocols · 2026Review
- Pharmacological targeting of kidney fibrosis: druggable mechanisms, translational models, and emerging antifibrotic therapies.Clinical kidney journal · 2026Review
- Mechanisms of fibrosis and novel antifibrotic therapies.EULAR rheumatology open · 2026Review
- A Hierarchical Hydrogel Modulates Immune-Mechanical Microenvironments to Spatiotemporally Reprogram Fibroblasts for Scarless Diabetic Wound Healing.Advanced healthcare materials · 2026Article
- Tubular La Ribonucleoprotein 7 Suppresses TGF- β /SMAD3 Signaling and Attenuates Kidney Fibrogenesis.Journal of the American Society of Nephrology : JASN · 2026Article
- Spatiotemporally Programmed Nanofiber Scaffold for Coordinated Hierarchical Multi-Tissue Regeneration in Pressure Ulcers.Advanced healthcare materials · 2026Article
- Inter-Organ Communication in Pulmonary Fibrosis: Systemic Modifiers of a Lung-Centered Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- A pan-tissue multi-omics resource atlas of coordinated immune, metabolic, and fibrotic alterations in diet-induced MASH.iScience · 2026Article
- TGFβ-1 induces the release of BAG3 protein by human fibroblasts.Journal of translational medicine · 2026Article
- Next-generation molecular imaging of cardiac fibrosis.The international journal of cardiovascular imaging · 2026Review
- Telomere-associated non-malignant pulmonary diseases: Pathogenic mechanisms and therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Matrix stiffness induced CREB3L1 activation contributed to skin fibrosis through calcium influx triggered endoplasmic reticulum stress.Cellular and molecular life sciences : CMLS · 2026Article
- 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
- Shared mechanisms of organ fibrosis.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
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 OpenQuestion 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 OpenQuestion graph.