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<p>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.</p>

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Neuroinflammation and RAMP1: the Role of the Peripheral and Central Nervous System in Tumor Progression

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月6日

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  • Pedro Daniel Moumesso Cavalcante,
  • Jonas Lucas Dias da Silva ,
  • Laryssa Rosy Santos Oliveira,
  • Rikelly Barbosa da Silva ,
  • Juliana Acioli Costa Lima ,
  • Guilherme de Brito Souza ,
  • Davi Ramon da Silva Santos ,
  • Júllia Victória Nascimento de Abrantes,
  • Mateus Lima de Farias ,
  • Sofia Amancio de Almeida Oliveira,
  • João Paulo Emiliano da Silva,
  • Rafael de Oliveira Calaça Farias,
  • Leonardo Prudêncio Coutinho de Almeida,
  • Salomão Belfort Sparapan de Melo,
  • Sandra Taveiros de Araújo ,
  • Raimundo Rodrigues de França-Júnior ,
  • José Emerson Xavier ,
  • Carlos Alberto de Carvalho Fraga

摘要

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.