ArticleJournal of translational medicine2025
FSTL1 accelerates nucleus pulposus-derived mesenchymal stem cell apoptosis in intervertebral disc degeneration by activating TGF-β-mediated Smad2/3 phosphorylation.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Awakening endogenous repair: salidroside boosts mitophagy in NPMSCs via SIRT1/FOXO3 to combat intervertebral disc degeneration.Stem cell research & therapy · 2026Article
- Signalling pathways regulated by FSTL1 in inflammation and potential therapeutic applications (Review).International journal of molecular medicine · 2026Review
- Multi-layered integrated shielding: engineering ferroptosis-resistant mesenchymal stem cells for precision therapy of intervertebral disc degeneration.Apoptosis : an international journal on programmed cell death · 2026Review
- PACS-2 Mitigates NPSC Apoptosis and Intervertebral Disc Degeneration by Preserving MAM Integrity via the SP1/LRRK2/Mfn2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ACE-mediated Glycosylation Stabilizes PSAP To Promote GPR37-dependent Macrophage-Nucleus Pulposus Cells Crosstalk and TGFβ Signaling in Alleviating Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntervertebral disc degeneration (IVDD) is the leading cause of low back pain, and repair using nucleus pulposus-derived mesenchymal stem cells (NP-MSCs) represents a promising therapeutic approach. However, both endogenous and transplanted NP-MSCs demonstrate limited proliferative capacity, increased apoptosis, and reduced resilience to the harsh microenvironment within the degenerative intervertebral disc (IVD).
methodsRNA sequencing (RNA-seq) was utilized to identify genes and associated mechanisms that mediate the responses of NP-MSCs to acidic conditions. Western blotting, qPCR, and immunofluorescence were used to evaluate follistatin-like 1 (FSTL1) expression in NP-MSCs. Apoptosis and extracellular matrix (ECM) anabolism were assessed via flow cytometry, TUNEL staining and Western blotting, while the TGF-β/Smad2/3 pathway was analyzed using Western blotting and immunofluorescence. FSTL1 knockdown with small interfering RNA (siRNA) was performed to determine its role in apoptosis and ECM regulation. The FSTL1 siRNA pretreatment was assessed in a puncture-induced rat IVDD model using MRI and histological staining.
resultsUsing RNA-seq, we identified FSTL1 as the primary acid-responsive gene in NP-MSCs. We further observed elevated FSTL1 expression in NP-MSCs isolated from degenerative IVDs in both humans and rats compared to normal IVDs. Acidic conditions upregulated FSTL1 expression in NP-MSCs in a pH-dependent manner. Notably, recombinant FSTL1 was shown to enhance cellular apoptosis and disrupt ECM metabolism. Conversely, silencing FSTL1 with siRNA reduced NP-MSC apoptosis and improved ECM anabolism. Importantly, TGF-β pathway inhibition partially reversed the pro-apoptotic and ECM catabolism effects of FSTL1. In the rat model of IVDD, pretreatment of NP-MSCs with FSTL1 siRNA significantly suppressed IVDD progression.
conclusionsThis study provides novel insights into the mechanistic role of FSTL1 in acid-induced apoptosis of NP-MSCs and its contribution to the progression of IVDD. These findings offer valuable perspectives for developing targeted therapeutic strategies to mitigate IVDD progression.
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.