ArticleNeurochemical research2025
Protective Effect of FABP5 Against 6-OHDA Induced Parkinson's Disease Via PPARγ/SIRT1/PGC-1α Signaling Pathway.
Article in Neurochemical research, 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
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
2 citing papers in PubMed.
- Curcumin and ferulic acid activate PPARγ-PGC1α signaling and improve mitochondrial function in a 6-OHDA-induced Parkinson's cellular model.Scientific reports · 2026Article
- The context-dependent roles of PPAR-γ in adipocyte differentiation and obesity: a master regulator with dual functions.Frontiers in nutrition · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Mitochondrial dysfunction of neurons is an important feature of Parkinson's disease (PD). Fatty acid binding protein 5 (FABP5) is a protein that regulates mitochondrial function and protects cell from neuronal injury. However, the potential of FABP5 administration to restore mitochondria has not been fully explored. In this study, PC12 cells and rats were induced by 6-hydroxydopamine (6-OHDA) to establish PD models. Our results showed that FABP5 promoted cell proliferation and protected against mitochondrial damage, and reduced apoptosis in vitro and vivo. Moreover, FABP5 treatment alleviates motor and non-motor symptom injury in vivo. It also effectively modulated the PPARγ/SIRT1/PGC-1α signaling pathway, thereby mitigating 6-OHDA-induced neurotoxicity. These results suggest that FABP5 exerts mitochondrial protection, inhibits apoptosis, restores damaged dopaminergic neurons, and slows down PD.
Indexed as
Identifiers
40445460What 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.