ReviewFrontiers in immunology2025
PI3K/Akt in IPF: untangling fibrosis and charting therapies.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed.
- ADAMTS14 is a novel modulator of fibroblast mechanoactivation in pulmonary fibrosis.American journal of respiratory and critical care medicine · 2026Article
- Mechanobiological feedback loops and quantitative decision thresholds in organ fibrosis: Translational principles for antifibrotic therapy.Journal of cell communication and signaling · 2026Review
- Nerandomilast (BI 1015550) attenuating pulmonary fibrosis in a mouse model of rheumatoid arthritis-associated interstitial lung disease by modulating the TGF-β1/PI3K/Akt signaling pathway.Journal of thoracic disease · 2026Article
- Chlorogenic Acid Attenuates Bleomycin-Induced Pulmonary Fibrosis in a Murine Model by Modulating TGF-β1 Expression.Advances in respiratory medicine · 2026Article
- Review
- Genetic determinants of drug-induced gingival overgrowth.Scientific reports · 2026Article
- Idiopathic pulmonary fibrosis from a multiscale mechanobiology perspective: Mechanisms and future therapeutic prospects.iScience · 2026Review
- Senescence-Driven Remodeling Defines an Aggressive and Immunomodulatory Subtype of Endometriosis.Aging cell · 2026Article
- Ivabradine Attenuates Experimental Hepatic Fibrosis by Modulating Inflammatory and Apoptotic Signaling Pathways.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Age-Dependent Alterations in Intestinal Barrier Function: Involvement of Microbiota and TLR4 Signaling.Biology · 2026Article
- A Multispecies, Modality-Agnostic Scalable In Vivo Mosaic Screening Platform for Therapeutic Target Discovery.bioRxiv : the preprint server for biology · 2026Article
- Myo-Inositol modulates AKT signalling, mitochondrial protein expression and intracellular Ca²⁺dynamics in human dermal fibroblasts.Scientific reports · 2026Article
- Synergistic regulation of TGF-β1/Smad2/3 signaling and inflammatory pathways via SA/NAC-based nanoplatforms: a novel strategy to enhance anti-fibrotic therapeutic outcomes in idiopathic pulmonary fibrosis.Journal of nanobiotechnology · 2026Article
- Machine Learning and Molecular Modeling for Drug Repurposing Targeting Potential PI3Kα Inhibitors in Post-CoViD-19 Pulmonary Fibrosis.ACS omega · 2026Article
- Rubiadin-1-methyl ether alleviates bleomycin induced pulmonary fibrosis.Scientific reports · 2026Article
- Nanoperlite Particles Enhance Fibrogenesis in Thyroid Orbital Fibroblasts: A Potential Activated Cell Source for Ocular Tissue Engineering.BioMed research international · 2026Article
- Astragalus Mongholicus for Idiopathic Pulmonary Fibrosis Treatment: From Molecules to Systems.Current molecular medicine · 2026Review
- An hiPSC-derived multi-lineage lung model exhibiting proximal-distal epithelial features for modeling pulmonary fibrosis.Frontiers in cell and developmental biology · 2026Article
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Three-dimensional-printed silk fibroin scaffolds loaded with adipose-derived stem cells prevent post endoscopic submucosal dissection esophageal stricture in a porcine model.Regenerative biomaterials · 2026Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive lung disease characterized by abnormal epithelial repair, persistent inflammation, and excessive extracellular matrix deposition, leading to irreversible scarring and respiratory failure. Central to its pathogenesis is the dysregulation of the PI3K/Akt signaling pathway, which drives fibroblast activation, epithelial-mesenchymal transition, apoptosis resistance, and cellular senescence. Senescent cells contribute to fibrosis through the secretion of pro-inflammatory and profibrotic factors in the senescence-associated secretory phenotype (SASP). Current antifibrotic therapies, Nintedanib and Pirfenidone, only slow disease progression and are limited by side effects, highlighting the need for novel treatments. This review focuses on the role of PI3K/Akt signaling in IPF pathogenesis, its intersection with inflammation and fibrosis, and emerging therapeutic approaches targeting molecules along this pathway.
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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 Socratic graph.