ArticleThe journal of spinal cord medicine2026
Heavy moxibustion at Sanyin point ameliorates neurogenic bladder dysfunction in spinal cord injury rats through the PI3 K/mTOR pathway.
Article in The journal of spinal cord medicine, 2026. 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.
- YS-49 activates the PI3K/AKT signaling pathway in MC3T3-E1 cells to enhance osteoblast differentiation and inhibits glucocorticoid-induced bone loss in vivo.BMC musculoskeletal disorders · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe present study aims to investigate the effect and mechanism of heavy moxibustion (100 moxa-cone) at Sanyin point (the common point of Yin and kidney) on the function of neurogenic bladder (NB) dysfunction in rats with spinal cord injury (SCI).
methodsTwenty-four male Sprague-Dawley rats were divided into four groups (n = 6): control, NB, NB + Moxibustion, and NB + Moxibustion + YS-49 (PI3 K agonist). The rats in control groups accepted a cut open of the skin, fascia, and muscle. The NB model was established using spinal cord transection. Fourteen days later, animals received heavy moxibustion at Sanyin point for three weeks or/and intraperitoneal administration of YS-49 (a PI3 K agonist). Basso, Beattie, and Bresnahan (BBB) scale, urodynamic parameters, bladder size, and weight were measured. The hematoxylin-eosin staining method was used to observe the histology of the bladder mucosa. Moreover, NB dysfunction after SCI could be restored by autophagy activation and autophagy is mediated by the PI3 K/Akt/mTOR pathway. Therefore, the expressions of autophagy factor (LC3 II/I and p62), PI3 K, and p-mTOR in the bladder mucosa were evaluated by western blotting.
resultsHeavy moxibustion treatment relieved the development of NB dysfunction in rats with SCI, with an increase in the bladder voiding efficiency and a decrease in afferent activity during storage in the moxibustion group compared with the NB group. The expression levels of LC3 II/I were markedly elevated by moxibustion, accompanied by a decrease in the levels of p62. YS-49 addition increased the PI3 K and p-mTOR expression which were down-regulated by moxibustion. Importantly, YS-49 reversed the effects of moxibustion on autophagy and bladder function.
conclusionHeavy moxibustion at Sanyin point exerted its effect on healing-impaired NB dysfunction in rats with SCI, possibly activating autophagy through the PI3 K/mTOR pathway.
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.