ArticleMolecular medicine reports2020
Overexpression of TIMP3 inhibits discogenic pain by suppressing angiogenesis and the expression of substance P in nucleus pulposus.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- An intelligent nanoliposome alleviates disc degeneration and discogenic pain by inhibiting neurovascular ingrowth via a "Soil-conditioning, seed-modulating, and weeds-suppressing" strategy.Bioactive materials · 2026Article
- Blood and lymphatic vascular remodeling in intervertebral disc degeneration.Frontiers in immunology · 2026Review
- What a pain in the back: etiology, diagnosis and future treatment directions for discogenic low back pain.Bone research · 2025Review
- Chronic Low Back Pain in Young Adults: Pathophysiological Aspects of Neuroinflammation and Degeneration.International journal of molecular sciences · 2025Article
- In vitro and ex vivo screening of microRNA combinations with enhanced cell penetrating peptides to stimulate intervertebral disc regeneration.JOR spine · 2024Article
- The Role of Microvascular Variations in the Process of Intervertebral Disk Degeneration and Its Regulatory Mechanisms: A Literature Review.Orthopaedic surgery · 2024Review
- Perineural Invasion Is Associated With Function-evoked Pain and Altered Extracellular Matrix in Patients With Head and Neck Squamous Cell Carcinoma.The journal of pain · 2024Article
- The pathogenesis and targeted therapies of intervertebral disc degeneration induced by cartilage endplate inflammation.Frontiers in cell and developmental biology · 2024Review
- Updates on Pathophysiology of Discogenic Back Pain.Journal of clinical medicine · 2023Review
- Inducing Angiogenesis in the Nucleus Pulposus.Cells · 2023Article
- Understanding painful versus non-painful dental pain in female and male patients: A transcriptomic analysis of human biopsies.PloS one · 2023Article
- Reactive Oxygen Species Mediate Low Back Pain by Upregulating Substance P in Intervertebral Disc Degeneration.Oxidative medicine and cellular longevity · 2021Article
- Melatonin prevents the binding of vascular endothelial growth factor to its receptor and promotes the expression of extracellular matrix-associated genes in nucleus pulposus cells.Experimental and therapeutic medicine · 2020Article
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Sensory neurons directly promote angiogenesis in response to inflammation via substance P signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 50% of the cases of low back pain (LBP) are attributed to discogenic origin. The causes of discogenic pain are complicated and consist of a complex biochemical cascade. Neovascularization of intervertebral discs (IVDs) is believed to be associated with discogenic pain. The anti‑angiogenesis ability of tissue inhibitor of metalloproteinase‑3 (TIMP3) has been reported in many tumors, yet whether TIMP3 is associated with neovascularization of IVDs remains unknown. In the present study, both in vitro and in vivo models were used to investigate the association between discogenic pain and TIMP3 expression in nucleus pulposus (NP). PCR results demonstrated that inflammation induced downregulation of TIMP3 expression in NP cells. By using an adenovirus system to upregulate TIMP3 expression, the effect of TIMP3 on angiogenesis was measured by endothelial cell migration and tube formation assays. The results demonstrated that overexpression of TIMP3 suppressed angiogenesis in NP without the regulation of vascular endothelial growth factor (VEGF) expression. TNF‑α converting enzyme (TACE) expression was downregulated by TIMP3, thus inhibiting the TACE‑induced activation of TNF‑α in NP cells. Immunohistochemical staining of IVDs also confirmed that TIMP3 inhibited the expression of substance P in NP. Taken together, the present results indicated the expression of TIMP3 in NP may have a key role in the development of discogenic pain.
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