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黄韧带纤维化和肥厚:分子途径、细胞机制及未来方向。

Ligamentum flavum fibrosis and hypertrophy: Molecular pathways, cellular mechanisms, and future directions.

机构信息

Department of Spine Surgery, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, China.

出版信息

FASEB J. 2020 Aug;34(8):9854-9868. doi: 10.1096/fj.202000635R. Epub 2020 Jul 1.

DOI:10.1096/fj.202000635R
PMID:32608536
Abstract

Hypertrophy of ligamentum flavum (LF), along with disk protrusion and facet joints degeneration, is associated with the development of lumbar spinal canal stenosis (LSCS). Of note, LF hypertrophy is deemed as an important cause of LSCS. Histologically, fibrosis is proved to be the main pathology of LF hypertrophy. Despite the numerous studies explored the mechanisms of LF fibrosis at the molecular and cellular levels, the exact mechanism remains unknown. It is suggested that pathophysiologic stimuli such as mechanical stress, aging, obesity, and some diseases are the causative factors. Then, many cytokines and growth factors secreted by LF cells and its surrounding tissues play different roles in activating the fibrotic response. Here, we summarize the current status of detailed knowledge available regarding the causative factors, pathology, molecular and cellular mechanisms implicated in LF fibrosis and hypertrophy, also focusing on the possible avenues for anti-fibrotic strategies.

摘要

黄韧带肥厚(LF)与椎间盘突出和小关节退变有关,是腰椎管狭窄症(LSCS)发展的原因。值得注意的是,LF 肥厚被认为是 LSCS 的一个重要原因。组织学上,纤维化被证明是 LF 肥厚的主要病理学改变。尽管有许多研究在分子和细胞水平上探讨了 LF 纤维化的机制,但确切的机制仍不清楚。有研究表明,机械应力、衰老、肥胖和某些疾病等病理生理刺激是致病因素。然后,LF 细胞及其周围组织分泌的许多细胞因子和生长因子在激活纤维反应中发挥不同的作用。在这里,我们总结了目前关于 LF 纤维化和肥厚的致病因素、病理学、分子和细胞机制的详细知识的现状,并重点关注抗纤维化策略的可能途径。

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ROCK-dependent mechanotransduction of macroscale forces drives fibrosis in degenerative spinal disease.由ROCK介导的宏观力机械转导驱动退行性脊柱疾病中的纤维化。
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Mechanical stress contributes to ligamentum flavum hypertrophy by inducing local inflammation and myofibroblast transition in the innovative surgical rabbit model.
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