Songhe Jiang

Cardiotoxicity induced by the chemotherapeutic agent Doxorubicin (Dox) is a major clinical challenge, primarily mediated by overwhelming oxidative stress. While Syringin (Syr) is known for its antioxidant potential, its efficacy and mechanism in the context of Dox‐induced cardiotoxicity are not well defined. This study aimed to assess the therapeutic potential of Syr in alleviating Dox‐induced cardiac injury and to elucidate its underlying molecular mechanism. The cardioprotective effect of Syr was evaluated in a Dox‐induced mouse model of cardiotoxicity and in primary cardiomyocytes, with pravastatin (Prv, 10 mg/kg) serving as the positive control in the Syr dose‐finding experiment. Cardiac function and myocardial strain were measured by advanced echocardiography using wall‐tracking and speckle‐tracking analyses. Network pharmacology was applied to identify downstream signaling pathways and molecular targets of Syr. Myocardial atrophy, antioxidant proteins, and oxidative stress markers were assessed by histology, Western blotting, and qRT‐PCR. To validate the key molecular target, in vivo siRNA‐mediated knockdown of the apelin receptor (APJ) was performed. Syr treatment significantly attenuated myocardial atrophy and suppressed oxidative stress. Syr also increased APJ expression, activated mechanosensitive PI3K/AKT phosphorylation, and restored fibroblast growth factor 21 (FGF21) homeostasis, thereby improving myocardial circumferential and longitudinal strain. Mechanistically, APJ silencing blunted Syr's ability to upregulate antioxidant proteins in Dox‐exposed cardiomyocytes, and the benefits of FGF21 overexpression were lost. Consistently, APJ knockdown abolished Syr's protection against Dox‐induced cardiotoxicity in vivo, eliminating its improvements in cardiac function and myocardial strain. Our study first demonstrates that Syr protects against Dox‐induced cardiotoxicity by restoring the APJ/PI3K/AKT signaling axis, which subsequently enhances the nuclear factor‐erythroid 2‐related factor 2/heme oxygenase‐1 (NRF2/HO‐1) antioxidant response and maintains FGF21 homeostasis. These findings identify Syr as a promising natural compound for mitigating chemotherapy‐induced cardiotoxicity and highlight the APJ as a novel therapeutic target.

Objective: Adolescent idiopathic scoliosis (AIS) necessitates multimodal management strategies integrating orthotic intervention and physiotherapeutic scoliosis‐specific exercises (PSSE). This study aimed to compare the clinical efficacy of brace therapy combined with tele‐rehabilitation‐guided PSSE versus brace treatment with self‐guided home‐based PSSE in mitigating spinal deformity progression. Methods: A cohort of 67 treatment‐naïve AIS patients from a tertiary scoliosis center (July 2021–July 2023) was stratified into two intervention groups: (1) tele‐rehabilitation (real‐time digitally supervised PSSE) and (2) autonomous practice (self‐guided home PSSE). Longitudinal evaluations at baseline, 6, 12, and 24‐month intervals included radiographic Cobb angle quantification, scoliometric angle of trunk rotation (ATR) assessment, and Scoliosis Research Society‐22 (SRS‐22) patient‐reported outcomes. Treatment success was categorized as improvement (Cobb reduction ≥ 5°), stability (change < 5°), or progression (increase ≥ 5°). Data were analyzed using paired and independent t ‐tests, Mann–Whitney U test, and Pearson's χ ² test. Results: At 24‐month follow‐up, the tele‐rehabilitation group exhibited significantly higher Cobb angle improvement rates (70.6% vs. 57.6%, p < 0.05) and lower progression rates (2.9% vs. 6.1%) compared to the autonomous practice group. Axial rotation correction demonstrated superior outcomes in the supervised cohort (final ATR: 6.9° ± 1.9° vs. baseline, p < 0.01). All SRS‐22 domains showed clinically meaningful improvements ( p < 0.05). Conclusion: Tele‐rehabilitation‐guided PSSE combined with bracing demonstrates enhanced efficacy over self‐guided protocols in achieving three‐dimensional deformity correction, stabilizing curve progression, and optimizing patient‐centered outcomes. Structured digital supervision emerges as a critical adjunct to orthotic management, advocating for technology‐integrated conservative strategies in adolescent spinal deformity care.

Parkinson’s disease, cognitive impairment, and multiple sclerosis are neurodegenerative conditions contributing to a huge health burden globally. Virtual reality rehabilitation has emerged as a promising intervention, but its comparative effectiveness across different types of neurodegenerative conditions must be further elucidated. Relevant studies were retrieved from the PubMed database, Cochrane Library, and Web of Science Core Collection database. Randomized controlled trials, meta-analyses, and systematic reviews investigating virtual reality interventions for neurodegenerative diseases were incorporated and evaluated. Following a thorough, methodical, and systematic screening process, 99 high-quality studies were ultimately incorporated. The findings corroborate the efficacy of immersive, semi-immersive, and non-immersive virtual reality interventions in cognitive and motor rehabilitation for patients with neurodegenerative diseases. Virtual reality rehabilitation shows great potential in improving motor function, cognitive function, and quality of life in patients with neurodegenerative diseases. Future research should focus on standardizing protocols and exploring the underlying neurobiological mechanisms to optimize its clinical use.

Objective: Few effective treatments improve upper extremity (UE) function after stroke. Immersive virtual reality (imVR) is a novel and promising strategy for stroke UE recovery. We assessed the extent to which imVR-based UE rehabilitation can augment conventional treatment and explored changes in brain functional connectivity (FC) that were related to the rehabilitation. Methods: An assessor-blinded, parallel-group randomized controlled trial was performed with 40 subjects randomly assigned to either imVR or Control group (1:1 allocation), each receiving rehabilitation 5 times per week for 3 weeks. Subjects in the imVR received both imVR and conventional rehabilitation, while those in the Control received conventional rehabilitation only. Our primary and secondary outcomes were the Fugl-Meyer assessment’s upper extremity subscale (FMA-UE) and the Barthel Index (BI), respectively. Both intention-to-treat (ITT) and per-protocol (PP) analyses were performed to assess the effectiveness of the trial. For both the FMA-UE/BI, a one-way analysis of covariance (ANCOVA) model was used, with the FMA-UE/BI at post-intervention or at follow-up, respectively, as the dependent variable, the two groups as the independent variable, baseline FMA-UE/BI, age, sex, site, time since onset, hypertension and diabetes as covariates. Results: Both ITT and PP analyses demonstrated the effectiveness of imVR-based rehabilitation. The FMA-UE score was greater in the imVR compared with the Control at the post-intervention (mean difference: 9.1 (95% CI 1.6, 16.6); P = 0.019) and follow-up (mean difference:11.5 (95% CI 1.9, 21.0); P = 0.020). The results were consistent for BI scores. Moreover, brain FC analysis found that the motor function improvements were associated with a change in degree in ipsilesional premotor cortex and ipsilesional dorsolateral prefrontal cortex immediately following the intervention and in ipsilesional visual region and ipsilesional middle frontal gyrus after the 12-week follow-up. Conclusions: ImVR-based rehabilitation is an effective tool that can improve the recovery of UE functional capabilities of subacute stroke patients when added to standard care. These improvements were associated with distinctive brain changes at two post-stroke timepoints. The study results will benefit future patients with stroke and provide evidence for a promising new method of stroke rehabilitation. Trial registration: ClinicalTrials.gov identifier: NCT03086889.

Previous studies have shown that peripheral nerve injury can lead to abnormal dendritic spine remodeling in spinal dorsal horn neurons. Inhibition of abnormal dendritic spine remodeling can relieve neuropathic pain. Electroacupuncture (EA) has a beneficial effect on the treatment of neuropathic pain, but the specific mechanism remains unclear. Evidence has shown that slit-robo GTPase activating protein 3 (srGAP3) and Rho GTPase (Rac1) play very important roles in dendritic spine remodeling. Here, we used srGAP3 siRNA and Rac1 activator CN04 to confirm the relationship between SrGAP3 and Rac1 and their roles in improving neuropathic pain with EA. Spinal nerve ligation (SNL) was used as the experimental model, and thermal withdrawal latency (TWL), mechanical withdrawal threshold (MWT), Western blotting, immunohistochemistry and Golgi-Cox staining were used to examine changes in behavioral performance, protein expression and dendritic spines. More dendritic spines and higher expression levels of srGAP3 were found in the initial phase of neuropathic pain. During the maintenance phase, dendritic spines were more mature, which was consistent with lower expression levels of srGAP3 and higher expression levels of Rac1-GTP. EA during the maintenance phase reduced the density and maturity of dendritic spines of rats with SNL, increased the levels of srGAP3 and reduced the levels of Rac1-GTP, while srGAP3 siRNA and CN04 reversed the therapeutic effects of EA. These results suggest that dendritic spines have different manifestations in different stages of neuropathic pain and that EA may inhibit the abnormal dendritic spine remodeling by regulating the srGAP3/Rac1 signaling pathway to alleviate neuropathic pain.