ArticlePhysiological reports2025
CIAPIN1 promotes proliferation and migration of PDGF-BB-activated airway smooth muscle cells via the PI3K/AKT and JAK2/STAT3 signaling pathways.
Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Regulatory networks of iron sulfur cluster biology in cancer mechanisms and therapeutic perspectives.iScience · 2026Review
- Midkine promotes PDGF-BB-induced proliferation, migration, and glycolysis of airway smooth muscle cells via the PI3K Akt pathway.Physiological reports · 2025Article
- CIAPIN1 promotes proliferation and migration of PDGF-BB-activated airway smooth muscle cells via the PI3K/AKT and JAK2/STAT3 signaling pathways.Physiological reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) is an essential anti-apoptotic protein; however, its role and associated molecular pathways in asthma remain largely unexplored. This study aimed to investigate the potential effects of CIAPIN1 on the proliferation and migration of platelet-derived growth factor BB (PDGF-BB)-induced ASMCs and the underlying mechanisms involved. Considering these aspects, ASMCs are activated with PDGF-BB as a cellular model for asthma. CIAPIN1 is then downregulated using small interfering ribonucleic acid (siRNA). Western blot analysis was performed to assess protein expression. Elevated levels of CIAPIN1 were observed, demonstrating a positive correlation with cytokine levels. CIAPIN1 expression is significantly increased in PDGF-BB-induced human ASMCs. In addition, CIAPIN1 knockdown inhibited proliferation, inflammatory cytokine production, and migration ability, while elevating apoptosis in PDGF-BB-induced human ASMCs. Moreover, CIAPIN1 knockdown inhibited phosphorylated phosphoinositide 3-kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), phosphorylated Janus kinase 2 (p-JAK2), and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) protein expression. In conclusion, the results indicate that CIAPIN1 regulates the proliferation and migration of human ASMC in response to PDGF-BB by inhibiting the PI3K/AKT and JAK2/STAT3 pathways.
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.