ReviewEuropean journal of medical research2025
Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.
Review in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Intervertebral disc degeneration (IVDD) is one of the main causes of chronic low back pain (LBP) and related spinal diseases, severely affecting patients' quality of life and imposing a considerable burden on healthcare systems. Current treatment strategies for IVDD primarily include conservative management and surgical intervention, but the therapeutic outcomes remain limited. Consequently, there is an urgent need to identify novel therapeutic targets. Recent research highlights the kallikrein-kinin system (KKS), a complex polypeptide network, as a key player in the pathological processes of IVDD. This review summarizes the multiple mechanisms by which KKS may contribute to IVDD, focusing on its involvement in mechanical stress, inflammatory responses, oxidative stress, cell proliferation and apoptosis, cellular senescence, extracellular matrix (ECM) degradation, angiogenesis, nerve ingrowth, nutrient supply, and genetic factors. Emerging evidence suggests that KKS exerts its functions largely through bradykinin 1 receptor (B1R) and bradykinin 2 receptor (B2R), regulating proinflammatory and oxidative processes, while also playing critical roles in apoptosis, senescence, and neovascularization. Furthermore, KKS is implicated in IVDD progression via modulation of calcium ion channels and key signaling pathways (e.g., NF-κB, MAPK, PI3K/Akt/mTOR). This review also discusses the role of KKS in IVDD-related pain mechanisms, highlighting its potential regulation of nerve growth factor (NGF) and subsequent modulation of pain perception. Collectively, these findings point to KKS as a promising therapeutic target for IVDD. Future studies should delve deeper into the local and systemic expression of KKS in intervertebral discs, develop targeted drugs against B1R and B2R, and evaluate their clinical efficacy and safety in IVDD treatment, thereby providing a theoretical foundation and novel strategies for more effective IVDD interventions.
Indexed as
Identifiers
What OpenQuestion holds
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.