Evidence mapPaperPMID 41226119Full record

ReviewMolecules (Basel, Switzerland)2025

Future Perspectives on Targeting the Activated TLR4/NFκB Pathway in Cystic Fibrosis: A Possible Interplay Between Ethnopharmacology and microRNA Therapeutics.

Roberto Gambari, Alessia Finotti

Abstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Roberto GambariDepartment of Life Sciences and Biotechnology, Ferrara University, I-44121 Ferrara, Italy.ORCID 0000-0001-9205-6033
Alessia FinottiDepartment of Life Sciences and Biotechnology, Ferrara University, I-44121 Ferrara, Italy.ORCID 0000-0002-7638-515X

Funding

Interuniversity Consortium for Biotechnologies, Italy (CIB) grant no. CIB-MUR-Unife2024
6 · The paper itself

Abstract

Cystic fibrosis (CF) is an inherited genetic disease caused by dysregulation of the cystic fibrosis transmembrane regulator (CFTR) gene, a chronic hyperinflammatory state and frequently occurring severe bacterial infections of the lungs. Novel protocols for treating CF inflammation are highly needed. Among the most interesting fields of pre-clinical investigation, the use of natural products, including those used in ethnopharmacology, appears to be promising. Examples of natural ethnopharmacological products that should be further investigated as potential anti-inflammatory agents for CF include inhibitors of the Toll-like receptor 4 (TLR4)/Nuclear Factor κB (TLR4/NFκB) pathway, such as parthenolide, curcumin and garlic-related constituents. In addition, "miRNA therapeutics" protocols have been reported as able to dampen the expression of pro-inflammatory genes. These two fields of investigation deserve, in the near future, further experimental efforts. Notably, these two approaches can be combined in order to develop novel strategies to improve the inhibitory activity on the expression of key pro-inflammatory genes activated in cystic fibrosis, including those induced by

Indexed as

Cystic FibrosisMicroRNAsNF-kappa BSignal TransductionToll-Like Receptor 4AnimalsAnti-Inflammatory AgentsCystic Fibrosis Transmembrane Conductance RegulatorHumansAnti-Inflammatory AgentsCystic Fibrosis Transmembrane Conductance RegulatorMicroRNAsNF-kappa BTLR4 protein, humanToll-Like Receptor 4garlicmicro RNAsnatural productsnuclear Factor-κBtoll-like receptor 4

Identifiers

PMID41226119
PMCPMC12608452

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.