The intervertebral disc (IVD) constitutes a critical organ within the spinal system, with the preservation of its homeostatic balance being essential for the integrity of the spinal mechanical apparatus. As age advances, the intervertebral discs are subject to a progressive degeneration influenced by a multitude of harmful stimuli, such as excessive axial or shear stresses, chemical stimuli, and biological factors. This degenerative process can precipitate a spectrum of spinal degenerative pathologies, including disc herniation, lumbar spinal stenosis, and lumbar spondylolisthesis. Consequently, such conditions may manifest clinically as low back pian, sciatica, or motor impairment in affected individuals.

During the dynamic process of intervertebral disc degeneration, its pathological morphology, pathophysiological mechanisms, cellular biology mechanisms, and key molecular markers all differ. Concurrently, the pathological structure and pathophysiological mechanisms of the intervertebral disc caused by stress stimuli, chemical stimuli, or biological stimuli must also exhibit numerous differences. Therefore, it is imperative that we investigate the pathological and pathophysiological structural alterations of the intervertebral discs under various detrimental stimuli across different age groups, thereby providing crucial evidence for the prevention, intervention, and treatment of intervertebral disc degeneration.

Conversely, the intervertebral disc possesses intrinsic mechanisms to modulate its homeostatic equilibrium, thereby counteracting the processes of degeneration. Within the disc's anatomical framework, the nucleus pulposus and its constituent cells perform pivotal biological functions, including the attenuation of excessive mechanical stress, the mediation of immune recognition and response to microbial stimuli, and the neutralization or elimination of chemical irritants. The exploration of this suite of intrinsic homeostatic regulatory mechanisms, coupled with the identification of pivotal protein targets, molecular biomarkers, and metabolites, can furnish essential theoretical and empirical substantiation for the innovation of novel pharmaceuticals, biomaterials, and avant-garde physicochemical therapeutic modalities.

This Research Topic focuses on the regulation of intervertebral disc homeostasis under various harmful stimuli. It also explores pathological morphological changes, pathophysiological alterations, key molecular targets, critical metabolic products, and novel biomarkers during the dynamic process of intervertebral disc degeneration. In addition, this topic investigates the molecular mechanisms underlying the intervertebral disc’s intrinsic homeostatic regulation under different stressors, providing a basis for the development of new drugs, biomaterials, and other innovative treatment approaches.

We welcome submissions of Original Research, Reviews, Mini-Reviews, and Perspectives that strengthen our understanding of the regulation of intervertebral disc homeostasis under microbial exposure or other harmful stimuli. The following subtopics are particularly encouraged:
• Exploration of pathological, pathophysiological, and cellular mechanisms, as well as biomarkers, during intervertebral disc degeneration or under different harmful stimuli.
• Identification of specific cellular receptors, key molecules, and mechanisms by which nucleus pulposus cells regulate intervertebral disc homeostasis.
• Development of innovative biomarkers, prognostic and predictive models, and quantitative analyses of pathological and pathobiological processes during intervertebral disc degeneration or under various harmful stimuli.
• Development of new drugs, bioengineered materials, or alternative strategies to regulate intervertebral disc or nucleus pulposus cell homeostasis to combat the degenerative process.
• Development of new drugs, bioengineered materials, or alternative strategies to treat disc degeneration and related degenerative conditions, such as low back pain and sciatica.

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Regulation of Intervertebral Disc Homeostasis and the Pathological or Pathophysiological Alterations Under Various Harmful Stimuli During Aging Process Volume II