Evidence map›Paper›PMID 39062196›Full record

ArticleBiomedicines2024

Inhibition of Protease-Activated Receptor-2 Activation in Parkinson's Disease Using 1-Piperidin Propionic Acid.

Santina Quarta, Michele Sandre, Mariagrazia Ruvoletto, Marta Campagnolo, Aron Emmi, Alessandra Biasiolo, Patrizia Pontisso, Angelo Antonini

Abstract read
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The Role of PAR2 in MASLD Progression and HCC Development.International journal of molecular sciences · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Santina QuartaDepartment of Medicine, University of Padova, 35122 Padova, Italy.ORCID 0000-0002-9348-1485
Michele SandreParkinson and Movement Disorders Unit, Padua Neuroscience Center (PNC), Center for Neurodegenerative Disease Research (CESNE), Department of Neuroscience, University of Padova, 35122 Padova, Italy.ORCID 0000-0002-3013-6908
Mariagrazia RuvolettoDepartment of Medicine, University of Padova, 35122 Padova, Italy.
Marta CampagnoloParkinson and Movement Disorders Unit, Padua Neuroscience Center (PNC), Center for Neurodegenerative Disease Research (CESNE), Department of Neuroscience, University of Padova, 35122 Padova, Italy.
Aron EmmiParkinson and Movement Disorders Unit, Padua Neuroscience Center (PNC), Center for Neurodegenerative Disease Research (CESNE), Department of Neuroscience, University of Padova, 35122 Padova, Italy.
Alessandra BiasioloDepartment of Medicine, University of Padova, 35122 Padova, Italy.
Patrizia PontissoDepartment of Medicine, University of Padova, 35122 Padova, Italy.ORCID 0000-0003-2077-9202
Angelo AntoniniParkinson and Movement Disorders Unit, Padua Neuroscience Center (PNC), Center for Neurodegenerative Disease Research (CESNE), Department of Neuroscience, University of Padova, 35122 Padova, Italy.ORCID 0000-0003-1040-2807

Funding

National Ministry of Health RF-2019-12369984
6 · The paper itself

Abstract

In Parkinson's disease, neuroinflammation is a double-edged sword; when inflammation occurs it can have harmful effects, despite its important role in battling infections and healing tissue. Once triggered by microglia, astrocytes acquire a reactive state and shift from supporting the survival of neurons to causing their destruction. Activated microglia and Proteinase-activated receptor-2 (PAR2) are key points in the regulation of neuroinflammation. 1-Piperidin Propionic Acid (1-PPA) has been recently described as a novel inhibitor of PAR2. The aim of our study was to evaluate the effect of 1-PPA in neuroinflammation and microglial activation in Parkinson's disease. Protein aggregates and PAR2 expression were analyzed using Thioflavin S assay and immunofluorescence in cultured human fibroblasts from Parkinson's patients, treated or untreated with 1-PPA. A significant decrease in amyloid aggregates was observed after 1-PPA treatment in all patients. A parallel decrease in PAR2 expression, which was higher in sporadic Parkinson's patients, was also observed both at the transcriptional and protein level. In addition, in mouse LPS-activated microglia, the inflammatory profile was significantly downregulated after 1-PPA treatment, with a remarkable decrease in IL-1β, IL-6, and TNF-α, together with a decreased expression of PAR2. In conclusion, 1-PPA determines the reduction in neuroglia inflammation and amyloid aggregates formation, suggesting that the pharmacological inhibition of PAR2 could be proposed as a novel strategy to control neuroinflammation.

Indexed as

microglianeurodegenerative diseasesneuroinflammationPAR2 inhibition

Identifiers

PMID39062196
PMCPMC11274518

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Registered trials

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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.