ArticleJournal of cellular and molecular medicine2025
HBP-A Attenuates Knee Osteoarthritis Progression via MLK3/P38/HDAC4 Axis-Mediated Dual Protection of Articular Cartilage and Quadriceps.
Article in Journal of cellular and molecular medicine, 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
15 authors.
Funding
Abstract
Knee osteoarthritis (KOA), a degenerative joint disease driven by biomechanical instability, involves cartilage degradation, muscle dysfunction, and MLK3/P38 MAPK pathway activation. Histone deacetylase 4 (HDAC4), a regulator of chondrocyte and muscle homeostasis, interacts with this pathway during disease progression. While Hyriopsis Bioactive Polysaccharide-Anodonta (HBP-A) exhibits P38 MAPK inhibitory properties in vitro, its in vivo therapeutic effects on musculoskeletal tissues remain uncharacterised. A destabilisation of the medial meniscus (DMM) mouse model was established to investigate HBP-A's therapeutic potential. Animals were randomly divided into sham-operated, DMM-induced, and HBP-A-treated groups. Following surgical induction, HBP-A (0.26 g/kg) was administered daily via oral gavage for 4 weeks. Comprehensive assessments included behavioural tests for pain sensitivity, micro-CT scanning, histological evaluation, and transmission electron microscope. Molecular mechanisms were investigated via immunohistochemical or immunofluorescence staining of MLK3, P38 MAPK, Caspase-3, and HDAC4, complemented by RT-qPCR analysis of myokine expression. HBP-A treatment significantly alleviated pain sensitivity compared to the DMM group. Structural evaluations revealed preserved subchondral bone integrity and attenuated cartilage degeneration, with histological scoring confirming reduced pathological changes. Quadriceps exhibited mitigated atrophy and restored ultrastructural organisation. Molecular profiling demonstrated suppressed MLK3/P38 MAPK pathway activation, diminished apoptotic activity, and elevated HDAC4 expression in both cartilage and quadriceps. HBP-A additionally normalised dysregulated expression of muscle-derived osteogenic factors linked to bone-cartilage crosstalk. These findings establish HBP-A as a dual-target therapeutic agent for KOA, concurrently mitigating cartilage and muscle degeneration through MLK3/P38 MAPK/HDAC4 axis modulation.
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.