We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
The Role of Oxidative Stress in Intervertebral Disc Degeneration
Summary
This review examined how oxidative stress contributes to the breakdown of intervertebral discs, a common condition that causes back pain. Researchers found that reactive oxygen and nitrogen species damage disc cells by promoting inflammation, cell death, and aging of the tissue. The study highlights that antioxidant therapies show promise for slowing disc degeneration, though proven treatment strategies remain limited.
Intervertebral disc degeneration is a very common type of degenerative disease causing severe socioeconomic impact, as well as a major cause of discogenic low back pain and herniated discs, placing a heavy burden on patients and the clinicians who treat them. IDD is known to be associating with a complex process involving in extracellular matrix and cellular damage, and in recent years, there is increasing evidence that oxidative stress is an important activation mechanism of IDD and that reactive oxygen and reactive nitrogen species regulate matrix metabolism, proinflammatory phenotype, autophagy and senescence in intervertebral disc cells, apoptosis, autophagy, and senescence. Despite the tremendous efforts of researchers within the field of IDD pathogenesis, the proven strategies to prevent and treat this disease are still very limited. Up to now, several antioxidants have been proved to be effective for alleviating IDD. In this article, we discussed that oxidative stress accelerates disc degeneration by influencing aging, inflammation, autophagy, and DNA methylation, and summarize some antioxidant therapeutic measures for IDD, indicating that antioxidant therapy for disc degeneration holds excellent promise.
Sign in to start a discussion.
More Papers Like This
The role of ageing and oxidative stress in intervertebral disc degeneration
This review details how aging and oxidative stress synergistically drive intervertebral disc degeneration through mitochondrial dysfunction, increased reactive oxygen species, and decreased antioxidant capacity. The progressive breakdown of disc matrix components under chronic oxidative damage suggests antioxidant therapies could potentially slow disc degeneration.
Polyethylene microplastics promote nucleus pulposus cell senescence by inducing oxidative stress via TLR4/NOX2 axis
Researchers found microplastics -- primarily polyethylene -- in nearly 60% of human spinal disc tissue samples, and lab studies showed these particles accelerate disc degeneration by triggering oxidative stress that causes disc cells to age prematurely. This is the first study to link microplastics directly to intervertebral disc disease, suggesting plastic pollution may contribute to back problems and spine deterioration.
From accumulation to degeneration: Microplastics as emerging risk factors for intervertebral disc health
Researchers reviewed evidence that microplastics accumulate in human intervertebral disc tissue at significantly higher concentrations (61 ± 44 particles/g) than in bone or cartilage, and discussed mechanisms by which this accumulation may contribute to disc degeneration.
Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 2.0/3.0
This editorial introduces a special issue focused on the cellular and molecular mechanisms behind oxidative stress in biological systems. Researchers highlight how the imbalance between reactive oxygen and nitrogen species and the body's antioxidant defenses contributes to a range of health conditions. The collection of studies aims to deepen understanding of oxidative stress pathways and potential therapeutic targets.
Microplastics and Oxidative Stress—Current Problems and Prospects
This review examines how microplastics cause oxidative stress, a condition where harmful molecules called free radicals damage cells. Microplastics have been linked to DNA damage, cell membrane disruption, mitochondrial problems, inflammation, and cell death, all driven by oxidative stress. These effects may contribute to serious health conditions including cancer and cardiovascular disease, though the authors note that more research is needed to fully understand the risks.