Cellular and molecular mechanisms of diabetes-mediated disc degeneration.

The aging population and lifestyle changes are contributing to a yearly increase in the incidence of spinal degenerative diseases, which significantly lead to chronic pain, neurological dysfunction, and diminished quality of life, with intervertebral disc degeneration as the fundamental pathological basis. Intervertebral disc degeneration, as the initiating factor of spinal degeneration, has always been the focus and difficulty of spine surgery. The typical intervertebral disc consists of the nucleus pulposus, annulus fibrosus, and cartilage endplate. Its nutrition primarily relies on the diffusion from the endplate, and its metabolic capacity is constrained, rendering it vulnerable to degenerative alterations caused by mechanical stress, aging, and metabolic influences. Recent studies indicate a strong correlation between diabetes mellitus and the onset and progression of intervertebral disc degeneration. As a global chronic metabolic disease, the metabolic disorders and vascular lesions caused by hyperglycemic state are closely related to spinal degenerative diseases, which makes diabetic patients face more complex spinal degeneration, and the degenerative process of intervertebral disc is accelerated and the degree of lesions is more severe. This article examines the cellular and molecular impacts of diabetic metabolic disorders on intervertebral disc degeneration, emphasizing the synergistic effects of inflammatory signaling, oxidative stress, extracellular matrix imbalance, and apoptosis. It elucidates the mechanisms by which these factors influence intervertebral disc degeneration, offering novel theoretical and practical insights for the prevention and treatment of spinal degenerative diseases, thereby furnishing patients with targeted treatment options and enhancing their quality of life.