ReviewActa pharmaceutica Sinica. B2022
Targeting PI3K/AKT signaling for treatment of idiopathic pulmonary fibrosis.
Review in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 2 of them syntheses that pooled it.
What it found
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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
257 citing papers in PubMed, 2 syntheses or guidelines pooled it, 411 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- Clinicopathological significance of AKT and phosphorylated AKT expression in hepatocellular carcinoma: A Meta-Analysis.BMC cancer · 2025Pooled it
- ADAMTS14 is a novel modulator of fibroblast mechanoactivation in pulmonary fibrosis.American journal of respiratory and critical care medicine · 2026Article
- M1 macrophage-derived CXCL12 drives neurogenic heterotopic ossification following spinal cord injury.Neural regeneration research · 2026Article
- PI3K-Akt signaling network crosstalk in cerebral ischemia/reperfusion injury: Mechanisms and therapeutic implications.Chinese medical journal · 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
- Targeting the PI3K/AKT/mTOR pathway in gastrointestinal cancers: a comprehensive review of mechanisms, preclinical evidence, and clinical challenges.Medical oncology (Northwood, London, England) · 2026Review
- Telomere-associated non-malignant pulmonary diseases: Pathogenic mechanisms and therapeutic strategies.Acta pharmaceutica Sinica. B · 2026Review
- Multi-omics Analysis Reveals the Prognostic and Therapeutic Value of TGF-β Signaling-related Genes in Idiopathic Pulmonary Fibrosis.Biochemical genetics · 2026Article
- Review
- CNOT9 affects hepatocellular carcinoma proliferation and cell cycle through the PTEN/AKT/p53 signaling pathway.Human cell · 2026Article
- ITGA7 interacts with FN1 to suppress the PI3K/AKT signaling pathway and inhibit thyroid cancer progression.Journal of cancer research and clinical oncology · 2026Article
- Unlocking the potential of mRNA nanomedicines for comprehensive fibrosis therapy.Molecular therapy. Nucleic acids · 2026Review
- Targeting the senescence‒autophagy axis via p16Signal transduction and targeted therapy · 2026Article
- The β-hydroxybutyrylation of Zyxin ameliorates pulmonary fibrosis by inhibiting lung fibroblast activation through the PI3K/AKT pathway.Respiratory research · 2026Article
- Inhibition of EIF2S1 expression regulates the PI3K/AKT pathway to mediate apoptosis in glioma cells: an in vitro study.Neurogenetics · 2026Article
- Osimertinib-induced interstitial lung disease insights from faers signal detection and network toxicology analysis.BMC cancer · 2026Article
- Epidermal PPARγ Signaling as a Suppressor of Toll-like Receptor-Mediated Inflammation and Fibrosis: Relevance to Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- Treatment of pulmonary fibrosis: From disease mechanisms to future novel therapies (Review).International journal of molecular medicine · 2026Review
- [Niranthin ameliorates Crohn's disease-like colitis in mice via antagonizing intestinal epithelial cell apoptosis and regulating intestinal Th1/Th2 immune homeostasis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
197 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic interstitial pneumonia with unknown causes. The incidence rate increases year by year and the prognosis is poor without cure. Recently, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT) signaling pathway can be considered as a master regulator for IPF. The contribution of the PI3K/AKT in fibrotic processes is increasingly prominent, with PI3K/AKT inhibitors currently under clinical evaluation in IPF. Therefore, PI3K/AKT represents a critical signaling node during fibrogenesis with potential implications for the development of novel anti-fibrotic strategies. This review epitomizes the progress that is being made in understanding the complex interpretation of the cause of IPF, and demonstrates that PI3K/AKT can directly participate to the greatest extent in the formation of IPF or cooperate with other pathways to promote the development of fibrosis. We further summarize promising PI3K/AKT inhibitors with IPF treatment benefits, including inhibitors in clinical trials and pre-clinical studies and natural products, and discuss how these inhibitors mitigate fibrotic progression to explore possible potential agents, which will help to develop effective treatment strategies for IPF in the near future.
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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 OpenQuestion graph.