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Article: Painful intervertebral disc degeneration and inflammation: from laboratory evidence to clinical interventions

TitlePainful intervertebral disc degeneration and inflammation: from laboratory evidence to clinical interventions
Authors
Issue Date2021
PublisherSpringer Nature, published in partnership with Sichuan University. The Journal's web site is located at ttp://www.nature.com/boneres/
Citation
Bone Research, 2021, v. 9, article no. 7 How to Cite?
AbstractLow back pain (LBP), as a leading cause of disability, is a common musculoskeletal disorder that results in major social and economic burdens. Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration, a significant contributor to LBP. Inflammatory mediators also play an indispensable role in discogenic LBP. The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies. Here, an overview of the advances in inflammation-related pain in disc degeneration is provided, with a discussion on the role of inflammation in IVD degeneration and pain induction. Puncture models, mechanical models, and spontaneous models as the main animal models to study painful disc degeneration are discussed, and the underlying signaling pathways are summarized. Furthermore, potential drug candidates, either under laboratory investigation or undergoing clinical trials, to suppress discogenic LBP by eliminating inflammation are explored. We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research.
Persistent Identifierhttp://hdl.handle.net/10722/305401
ISSN
2021 Impact Factor: 13.362
2020 SCImago Journal Rankings: 3.289
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLyu, F-
dc.contributor.authorCui, H-
dc.contributor.authorPan, H-
dc.contributor.authorCheung, KMC-
dc.contributor.authorCao, X-
dc.contributor.authorIatridis, JC-
dc.contributor.authorZheng, Z-
dc.date.accessioned2021-10-20T10:08:53Z-
dc.date.available2021-10-20T10:08:53Z-
dc.date.issued2021-
dc.identifier.citationBone Research, 2021, v. 9, article no. 7-
dc.identifier.issn2095-4700-
dc.identifier.urihttp://hdl.handle.net/10722/305401-
dc.description.abstractLow back pain (LBP), as a leading cause of disability, is a common musculoskeletal disorder that results in major social and economic burdens. Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration, a significant contributor to LBP. Inflammatory mediators also play an indispensable role in discogenic LBP. The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies. Here, an overview of the advances in inflammation-related pain in disc degeneration is provided, with a discussion on the role of inflammation in IVD degeneration and pain induction. Puncture models, mechanical models, and spontaneous models as the main animal models to study painful disc degeneration are discussed, and the underlying signaling pathways are summarized. Furthermore, potential drug candidates, either under laboratory investigation or undergoing clinical trials, to suppress discogenic LBP by eliminating inflammation are explored. We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research.-
dc.languageeng-
dc.publisherSpringer Nature, published in partnership with Sichuan University. The Journal's web site is located at ttp://www.nature.com/boneres/-
dc.relation.ispartofBone Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titlePainful intervertebral disc degeneration and inflammation: from laboratory evidence to clinical interventions-
dc.typeArticle-
dc.identifier.emailCheung, KMC: cheungmc@hku.hk-
dc.identifier.authorityCheung, KMC=rp00387-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41413-020-00125-x-
dc.identifier.pmid33514693-
dc.identifier.pmcidPMC7846842-
dc.identifier.scopuseid_2-s2.0-85100092178-
dc.identifier.hkuros327446-
dc.identifier.volume9-
dc.identifier.spagearticle no. 7-
dc.identifier.epagearticle no. 7-
dc.identifier.isiWOS:000613473200001-
dc.publisher.placeChina-

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