ReviewNeurochemical research2025
Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis.
Review in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Mesenchymal Stem Cell-Derived Exosomes: A Promising Therapeutic Strategy for Spinal Cord Injury.International journal of nanomedicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The intricate pathophysiological cascades following spinal cord injury (SCI), encompassing cellular demise, axonal degeneration, and the formation of glial scars, pose formidable barriers to neural regeneration and restoration. Notably, neuroinflammation and glial scars emerge as pivotal barrier to post-SCI repair. Formyl peptide receptors (FPRs) emerge as critical regulators of immune responses, exerting significant influence over inflammatory modulation and nerve regeneration subsequent to SCI. Beyond their classical expression in myeloid cells, FPRs demonstrate a pronounced presence within the central nervous system (CNS) with roles in the progression of neurodegenerative disorders and neurological malignancies. Post-SCI, the equilibrium of the inflammatory microenvironment is recalibrated through the strategic modulation of FPRs, including facilitating a balance in microglial polarization, stimulating neural stem cells (NSCs) migration, and promoting neural axon elongation. These observations enlighten the potential of FPRs as innovative targets for neuronal regenerations bolstering SCI repair. This review endeavors to delineate the distribution and function of FPRs in the aftermath of SCI, with a special attention to their roles in inflammatory regulation, NSCs mobilization, and synaptic growth. By elucidating these mechanisms, we aspire to contribute novel insights and strategies for SCI therapy.
Indexed as
Identifiers
39920516What 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.