ArticleEndocrine, metabolic & immune disorders drug targets2026
The effects of Tissue-type Plasminogen Activator on PSC Activation.
Article in Endocrine, metabolic & immune disorders drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionOur previous studies have demonstrated that the activated pancreatic stellate cell (PSC) could induce islet damage in type 2 diabetes mellitus (T2DM). While tissue-type plasminogen activator (tPA) is significantly reduced in T2DM, its subsequent effects are unclear. The purpose of this experiment was to observe the impact of tPA on PSC activation, with the aim to better understand the potential role of tPA in T2DM.
methods50 type 2 diabetic patients and 50 healthy persons were included in the diabetic group and the control group, respectively. Fasting blood was collected separately, and the tPA-level was detected by ELISA. Rat PSCs were isolated from pancreatic tissue using standard explant techniques. The PSCs were then characterized by staining them with Oil Red O to visualize lipid droplets and using immunofluorescent markers (α-smooth muscle actin (α-SMA), vimentin, and glial fibrillary acidic protein (GFAP)). After characterization, the PSCs were treated with tPA, then the proliferation of PSCs was measured using the cell counting kit-8 (CCK-8), the apoptosis was observed by the caspase-3 fluorometric assay kit, and the migration ability was assessed using the wound-healing assay and the transwell migration assay. Finally, a Western blot was used to identify the extracellular matrix (ECM) component synthesized by PSCs.
resultsThe diabetic patients had significantly lower levels of tPA compared to the controls. Rat PSCs treated with tPA exhibited more lipid droplet accumulation, and their ability of proliferation, migration, and ECM synthesis were significantly inhibited. DISCUSSION: These findings suggest that tPA may serve as an endogenous suppressor of PSC activation, and its deficiency in T2DM likely contributes to islet fibrosis and progressive β-cell dysfunction.
conclusionThis study demonstrated that tPA can play a crucial role in significantly inhibiting the activation, proliferation, migration, and ECM synthesis of PSC. Therefore, we speculate that the significant reduction of tPA in T2DM may exacerbate the detrimental effect of PSC on β-cell function.
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.