Por favor, use este identificador para citar o enlazar este ítem: DOI 10.14670/HH-11-846

Título: Inflammatory mediators and signalling pathways controlling intervertebral disc degeneration
Fecha de publicación: 2017
Editorial: Universidad de Murcia. Departamento de Biología Celular e Histología
Cita bibliográfica: Histology and Histopathology, Vol.32, nº6, (2017)
ISSN: 1699-5848
0213-3911
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: Intervertebral disc degeneration
Inflammatory mediators
Low back pain
Neuroinflammation
Resumen: Intervertebral disc (IVD) degeneration (IDD) is one of the major causes of back pain, a condition that represents a serious socio-economic burden. Deeper knowledge of the complex and fine relationship between IVD degeneration, tissue inflammation and pain, appears to be critical to improve the current therapies, which have so far proven themselves ineffective. Upon degeneration, IVD tissues become inflamed, and this inflammatory microenvironment is associated with a cascade of degenerative events that may eventually cause discogenic pain. In particular, several studies have highlighted the major role of a number of proinflammatory mediators not only in the onset of the inflammatory condition, but also in the development of IDD in general. In this review, we will present the main pathological events that occur during disc degeneration, focusing on the relationship between the abnormal inflammatory milieu of the degenerating IVD, IDD and the generation of pain. Finally, we will present the current therapies for the treatment of IDD and low back pain, and the perspectives of future, more effective therapies.
Autor/es principal/es: Navone, Stefania Elena
Marfia, Giovanni
Giannoni, Amedeo
Beretta, Matteo
Guarnaccia, Laura
Gualtierotti, Roberta
Nicoli, Daniele
Rampini, Paolo
Campanella, Rolando
URI: http://hdl.handle.net/10201/117227
DOI: DOI 10.14670/HH-11-846
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 20
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Aparece en las colecciones:Vol.32, nº6 (2017)

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