ArticleApoptosis : an international journal on programmed cell death2025
Mechanism of glycolysis-pyrolysis crosstalk driving vicious circle of intervertebral disc degeneration.
Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Ammonia Accumulation Drives Intervertebral Disc Degeneration by Triggering Ammonia-Induced Cell Death Through Lysosome-Mitochondria Crosstalk.Cell proliferation · 2026Article
- TRIM25 facilitates mitochondrial dysfunction and extracellular matrix degradation by enhancing USP7-driven ENO1 deubiquitination during intervertebral disc degeneration.Clinical and translational medicine · 2026Article
- The emerging role of lactate in skeletal homeostasis and disorders: Integrated mechanisms and translational opportunities.Journal of orthopaedic translation · 2026Review
- Metabolic Dysregulation of FC3 Fibrochondrocytes via MDH2 Promotes Intervertebral Disc Degeneration.Journal of cellular and molecular medicine · 2026Article
- Beyond the hype: the glycolysis-pyroptosis axis in intervertebral disc degeneration and the path to therapeutic translation.Apoptosis : an international journal on programmed cell death · 2026Article
- Mechanism-guided biomaterial strategies for intervertebral disc degeneration: Pathological heterogeneity, functional classification, and translational perspectives.Journal of tissue engineeringReview
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
The acidic and inflammatory microenvironment serves as a central pathological feature of intervertebral disc degeneration (IVDD), acting as a critical driving factor in disease progression. However, the interplay between acidic and inflammatory microenvironments remains largely unexplored. In this study, we revealed the molecular mechanism by which crosstalk between glycolysis and pyroptosis exacerbates IVDD. We observed that lactic acid stimulation triggers pyroptosis in NPCs by stimulating the NLRP3 inflammasome, activating the caspase-1 pathway, and upregulating the expressions of IL-1β and IL-18. Acid sensitive ion channel 1a (ASIC1a) expression is positively correlated with extracellular acidosis severity and NPC pyroptosis levels. Furthermore, the knockdown of ASIC1a via siRNA effectively alleviated pyroptosis. After treatment of NPCs with IL-1β, glycolysis levels were increased, accompanied by up-regulation of c-Myc (a key regulator of the Warburg effect) and nuclear translocation, the knockdown of c-Myc effectively alleviated glycolysis. Mechanistically, lactate activates acid-sensing ion channel 1a (ASIC1a), which mediates Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.