Lactylation driven by lactate metabolism in the disc accelerates intervertebral disc degeneration: A hypothesis
Lactylation driven by lactate metabolism in the disc accelerates intervertebral disc degeneration: A hypothesis
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DOI：
10.1016/j.mehy.2021.110758
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发表时间：
2022-01-06
影响因子：
4.7
通讯作者：
Wu, Xinghuo
中科院分区：
文献类型：
--
作者：
Cheng, Chuan;Xu, Zhiqiang;Wu, Xinghuo
细胞内动态平衡失衡与椎间盘退变密切相关。乳酸是糖酵解的最终产物，是IDD潜在的生物标志物。乳酸转运代谢紊乱可显著升高乳酸浓度，影响细胞外基质的酸度，是导致椎间盘和IDD内酸性环境的主要原因。乳酸的代谢功能已被深入研究，但其非代谢功能仍不清楚。新发现的组蛋白乳糖化修饰为探讨IDD的发病机制提供了新的思路。乳酸的产生和积聚导致了组蛋白乳糖化修饰水平的升高。此外，它还会影响基因组水平的转录调控，调节髓核细胞的功能和命运，导致椎间盘退变的发生和发展。在IDD过程中，乳酸的产生和组蛋白的乳糖化修饰可能是IDD的重要调节机制，值得进一步研究。
The imbalance of intracellular homeostasis is closely related to intervertebral disc degeneration (IDD). Lactate, the final product of glycolysis, is a potential biomarker of IDD. The disorder of lactate transport and metabolism can significantly increase the concentration of lactate and affect the acidity of extracellular matrix, which is the main cause of the acidic environment in the disc and IDD. The metabolic function of lactate has been studied in depth, but its non-metabolic function is still unclear. The newly discovered modification of histone lactylation provides a new idea for the mechanism of IDD. The production and accumulation of lactate results in increased modification level of histone lactylation in intervertebral disc. Furthermore, it will affect genome-level transcriptional regulation, regulate the function and fate of nucleus pulposus cells, and lead to the occurrence and development of intervertebral disc degeneration. During the process of IDD, lactate production and histone lactylation modification may be an important regulatory mechanism of IDD, which is worthy of further investigation.