지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2022.3
- 수록면
- 199 - 210 (12page)
- DOI
- 10.3349/ymj.2022.63.3.199
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초록· 키워드
오류제보하기
Intervertebral disc (IVD) degeneration is the main source of intractable lower back pain, and symptomatic IVD degenerationcould be due to different degeneration mechanisms. In this article, we describe the molecular basis of symptomatic IVD degenerativedisc diseases (DDDs), emphasizing the role of degeneration, inflammation, angiogenesis, and extracellular matrix (ECM)regulation during this process. In symptomatic DDD, pro-inflammatory mediators modulate catabolic reactions, resulting inchanges in ECM homeostasis and, finally, neural/vascular ingrowth-related chronic intractable discogenic pain. In ECM homeostasis,anabolic protein-regulating genes show reduced expression and changes in ECM production, while matrix metalloproteinasegene expression increases and results in aggressive ECM degradation. The resultant loss of normal IVD viscoelasticity and a concomitantchange in ECM composition are key mechanisms in DDDs. During inflammation, a macrophage-related cascade is representedby the secretion of high levels of pro-inflammatory cytokines, which induce inflammation. Aberrant angiogenesis is considereda key initiative pathologic step in symptomatic DDD. In reflection of angiogenesis, vascular endothelial growth factorexpression is regulated by hypoxia-inducible factor-1 in the hypoxic conditions of IVDs. Furthermore, IVD cells undergoing degenerationpotentially enhance neovascularization by secreting large amounts of angiogenic cytokines, which penetrate the IVD fromthe outer annulus fibrosus, extending deep into the outer part of the nucleus pulposus. Based on current knowledge, a multi-disciplinaryapproach is needed in all aspects of spinal research, starting from basic research to clinical applications, as this will provideinformation regarding treatments for DDDs and discogenic pain.
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