ArticleMolecular and cellular biochemistry2025
GDF15 attenuates Parkinson's disease progression via suppressing the activation of cGAS-STING pathway.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
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Who cites it
2 citing papers in PubMed.
- Role and mechanisms of ferroptosis in cognitive impairment: From molecular pathways to therapeutic targets (Review).International journal of molecular medicine · 2026Review
- Chronic and non-canonical cGAS-STING activation: implications for health, disease, cancer, and emerging therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth differentiation Factor 15 (GDF15) plays an important role in the innate immune response. However, whether GDF15 could regulate Parkinson's disease (PD) remains unknown. In this study, we explored the function and underlying molecular mechanisms of GDF15 in PD. The protein and mRNA expressions were examined applying immunofluorescence staining, Western blot and qRT-PCR. Ferrous iron content was also assessed using an iron assay kit. The effect of GDF15 knockdown on mitochondrial membrane potential, ROS level, intracellular Fe
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40178669What Socratic holds
Registered trials
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