ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Inhibition of Hypersialylation in Human Intervertebral Disc Degeneration Modulates Inflammation and Metabolism.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Article
- Inhibition of Hypersialylation in Human Intervertebral Disc Degeneration Modulates Inflammation and Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
Intervertebral disc (IVD) degeneration is a major cause of low back pain (LBP), a significant global health burden. While glycosylation plays a key role in cellular signaling and inflammation, its role in IVD degeneration remains poorly understood. This study characterizes glycan alterations in human healthy and degenerated IVDs using glycomic (UPLC-MS, MALDI-IMS) and proteomic (LC-MS) analyses, combined with functional studies. These results identify hypersialylation, especially α-2,6-linked sialic acid, as a prominent feature of degenerated IVDs. In vitro inhibition of sialylation (3Fax-peracetyl Neu5Ac) in nucleus pulposus cells demonstrates reduced oxidative stress and inflammatory signaling, indicating a functional role for hypersialylation in IVD pathology. Targeting glycosylation pathways, notably sialylation, emerges as a promising therapeutic strategy for IVD degeneration.
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Registered trials
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