ReviewCell biochemistry and biophysics2026
Neuroinflammation and RAMP1: the Role of the Peripheral and Central Nervous System in Tumor Progression.
Review in Cell biochemistry and biophysics, 2026. 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.
- CGRP: the immune system's double agent - context-dependent roles in inflammation, resolution and cancer.Frontiers in immunology · 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
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcitonin gene-related peptide (CGRP) and receptor activity modifier protein 1 (RAMP1) form a critical neuroimmunoendocrine axis in the modulation of neuroinflammation, pain, and tumor progression. CGRP, released by sensory and sympathetic fibers, is a potent vasodilator and nociceptive modulator; its action depends on the receptor composed of CALCRL and RAMP1. In the central nervous system, the activation of microglia and astrocytes and the induction of pathways such as NF-κB and MAPK culminate in the production of proinflammatory cytokines (TNF-α, IL-6), differing from systemic inflammation due to the presence of the blood-brain barrier and the glial microenvironment. Preclinical evidence demonstrates RAMP1 expression in neurons, glial cells, endothelium, and macrophages; CGRP/RAMP1 signaling promotes vascular permeability, cytokine release, and angiogenesis, potentially synergizing with VEGF. In animal models and cell cultures, genetic or pharmacological manipulations of the axis reduce tumor angiogenesis, pro-tumor immune infiltration, tumor growth, and nociceptive behavior. Given the clinical availability of CGRP antagonists and monoclonal antibodies, blocking the CGRP/RAMP1 axis is a promising translational strategy for modulating tumor progression and cancer pain. This review summarizes preclinical evidence on mechanisms and therapeutic feasibility. The article includes preclinical and clinical safety and biomarker studies.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.