Chengdu University of Traditional Chinese Medicine

This study explored mental workload recognition methods for carrier-based aircraft pilots utilising multiple sensor physiological signal fusion and portable devices. A simulation carrier-based aircraft flight experiment was designed, and subjective mental workload scores and electroencephalogram (EEG) and photoplethysmogram (PPG) signals from six pilot cadets were collected using NASA Task Load Index (NASA-TLX) and portable devices. The subjective scores of the pilots in three flight phases were used to label the data into three mental workload levels. Features from the physiological signals were extracted, and the interrelations between mental workload and physiological indicators were evaluated. Machine learning and deep learning algorithms were used to classify the pilots’ mental workload. The performances of the single-modal method and multimodal fusion methods were investigated. The results showed that the multimodal fusion methods outperformed the single-modal methods, achieving higher accuracy, precision, recall and F1 score. Among all the classifiers, the random forest classifier with feature-level fusion obtained the best results, with an accuracy of 97.69%, precision of 98.08%, recall of 96.98% and F1 score of 97.44%. The findings of this study demonstrate the effectiveness and feasibility of the proposed method, offering insights into mental workload management and the enhancement of flight safety for carrier-based aircraft pilots.

Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory autoimmune disease of the central nervous system, in which aquaporin-4 immunoglobulin G (AQP4-IgG) targets the water channel aquaporin-4 (AQP4) localized at astrocytic endfeet, thus triggering inflammatory lesions and tissue damage. The pathological characteristics of NMOSD are early loss of oligodendrocytes, extensive demyelination, and axonal injury. The pathogenesis of oligodendrocyte damage in NMOSD includes complement-dependent bystander effect, antibody-dependent cell-mediated cytotoxicity bystander effect, glutamate toxicity, connexin dysregulation, and blood-brain barrier disruption. Remyelination levels in acute NMOSD lesions are low.

Background Treatment options for intracranial atherosclerotic stenosis (ICAS) are limited, but endovascular intervention has gained increasing attention in recent years. Aim To evaluate the safety and efficacy of the Neuroform EZ stent for treating ICAS in the posterior circulation. Material & methods Patients’ (n = 50) eligibility depended on ICAS with severe stenosis (≥ 70%) in the intracranial segment of the vertebral artery or basilar artery shown by cerebral angiography. General information of the participants were recorded, Adverse events during the perioperative period were observed, including in-stent thrombosis, postoperative hyperperfusion, stroke, and mortality. Before the procedure, neurological deficits (NIHSS score) and neurological recovery (mRS score) were recorded at 12 months postoperatively. The degree of vascular stenosis was evaluated prior to and following the procedure, and in-stent restenosis (ISR) was recorded at 12 months post-operation. Results Fifty-two stents were successfully placed in 50 patients, followed by standardized medication. Angiographic follow-up was completed 12-months postoperatively, and there was only one case of ISR (4.35%) was observed. Postoperative stenosis of responsible vessel was significantly relieved (77.98 ± 7.69 vs. 33.85 ± 9.11), with statistically significant differences (P < 0.01). The extent of neurological deficits and effects on daily living activities at 12 months postoperatively exhibited significant improvements, as evidenced by NIHSS scores (2.40 ± 1.37 vs. 0.82 ± 0.77) and mRS scores ≤ 2 (82.0% vs. 98.0%) (P < 0.01). Cerebral perfusion improved, with no significant perioperative complications. Conclusions The Neuroform EZ stent is a safe and effective treatment approach for ICAS in the posterior circulation.

Immunotherapy has become the standard treatment for many types of cancers, but an increasing number of patients who initially respond to these treatments develop acquired immunotherapy resistance (AIR). Here, we recapitulated the entire process of immunotherapy from response to AIR in mice with non–small cell lung cancer (NSCLC). With implanted tumor organoids derived from these models and serial transplants, we demonstrated that tumor cell–intrinsic mechanisms contributed significantly to AIR. Single-cell RNA sequencing and electron microscope assays revealed that resistant tumor cell–expressing collagens, including Col3a1 and Col6a1 , formed multiple physical barriers surrounding tumor cells. Disruption of these barriers by collagenase or knockout of both Col3a1 and Col6a1 in tumor cells could sensitize the tumors of AIR. Mechanistically, the TGFβ pathway was upregulated upon immunotherapy, and treatment with TGFβ significantly increased the expression levels of both Col3a1 and Col6a1 in tumor cells. COL3A1 formed a castle-like barrier for a cluster of tumor cells and prevented T cell infiltration, while COL6A1 formed an armor-like barrier surrounding individual tumor cells to protect them against direct T cell attack. Our data reveal a tumor cell–intrinsic mechanism of AIR, mediated by collagen-containing physical barriers, which immediately suggests a clinical treatment option.

Introduction Yellow urticaria (YU) is a rare variant of urticaria characterized by a transient yellow rash. It usually occurs at patients with hyperbilirubinemia. In clinic, the vasodilation and extravasation associated with urticaria facilitate the precipitation of bilirubin within the elastin fibers of the cutaneous tissue, which consequently leads to the emergence of atypical yellow papules and plaques. The occurrence of hyperbilirubinemia in cases of yellow urticaria is commonly attributed to underlying liver diseases, including infectious hepatitis, metastatic disease of the liver, liver cirrhosis due to various causes. Here, we report a case of YU secondary to platelet transfusion. Purpose Red and purple rashes are common, whereas yellow wheals are rarely reported. Therefore, we are supposed to keep an eye on the diagnosis of YU. Patients and Methods We present a case of YU secondary to platelet transfusion that responds rapidly to anti-hypersensitive and antihistamine treatment. Results Based on the skin lesion and histopathology result, we considered that the patient developed YU. The patient with YU responds rapidly to anti-hypersensitive and antihistamine treatments, with no adverse effects or recurrence. The prognosis of YU is with favorable outcome. It seldom turns into chronic urticaria and occurs repeatedly. Conclusion The exact pathogenesis of yellow urticaria remains uncertain. It has been proposed that the yellow coloration of the disease may result from the increased capillary permeability that cytokines and mediators, especially histamine, induce. Yellow hives are attributed to underlying hyperbilirubinemia with skin deposits and suggest underlying causes, particularly liver diseases. Conventional anti-hypersensitive and antihistamine treatments are effective in treating YU. Prophylactic and systematical use of antihistamine agents may prevent relapse.

Exosomes, lipid bilayer nanovesicles secreted by nearly all cell types, play pivotal roles in intercellular communication by transferring proteins, nucleic acids, and lipids. This review comprehensively summarizes their multiple functions in inflammation and cancer. In inflammation, exosomes exhibit context-dependent pro- or anti-inflammatory effects: they promote acute responses by delivering cytokines and miRNAs to activate immune cells, yet suppress chronic inflammation via immunoregulatory molecules. Two representative inflammatory diseases, namely sepsis and inflammatory bowel disease, were highlighted to elucidate their roles in the acute and chronic inflammatory diseases. In cancer, exosomes orchestrate tumor microenvironment (TME) remodeling by facilitating angiogenesis, metastasis, and immune evasion through interactions with cancer-associated fibroblasts, tumor-associated macrophages, and extracellular matrix components. Furthermore, exosomes can facilitate the transition from inflammation to cancer by impacting pertinent signaling pathways via their transported oncogenic and inflammatory molecules. Tumor-derived exosomes also serve as non-invasive biomarkers correlating with disease progression. Clinically, exosomes demonstrate promise as therapeutic agents and drug carriers, evidenced by ongoing trials targeting inflammatory diseases and cancers. However, challenges in isolation standardization, scalable production, and understanding functional heterogeneity hinder clinical translation. Future research should prioritize elucidating cargo-specific mechanisms, optimizing engineering strategies, and advancing personalized exosome-based therapies. By bridging molecular insights with clinical applications, exosomes hold great potential in precision medicine for inflammation and oncology.

To investigate the inhibitory effects and underlying mechanisms of Qideng Mingmu Capsules (QD) on retinal neovascularization (RNV). Seven-day-old C57BL/6J mice were assigned to the following groups: control, oxygen-induced retinopathy (OIR), low-, medium-, high-dose QD (225, 450, and 900 mg/g daily), and angiopoietin 1 (Ang1), 20 mice in each group. Except for the control group, an OIR model was induced by exposing mice to a hyperoxic environment for 5 d (postnatal days 7–12), followed by a normoxic environment for 5 d (postnatal days 12–17). From day 12, the treatment groups received QD orally or Ang1 via binocular intravitreal injection. On day 17, hematoxylin and eosin staining and fluorescein isothiocyanate-dextran staining were performed to evaluate RNV growth. Immunofluorescence staining, immunohistochemistry, and Western blotting were used to analyze the expressions of Ang/tyrosine kinase with immunoglobulin and epidermal growth factor homology domain-2 (Tie2) signaling pathway, hypoxia-inducible factor-1α (HIF-1α), and retinal vascular maturation markers. In addition, the effects of QD on the viability of rat retinal microvascular endothelial cells (rRMECs) was assessed. QD significantly inhibited RNV formation, reduced RNV density, increased the expressions of Ang1, Tie2, and phosphorylated protein kinase B, and decreased the expression of Ang2 (P<0.05 or P<0.01). QD also enhanced retinal vascular pericyte coverage, reduced HIF-1α expression, and increased vascular endothelial cadherin levels (P<0.05 or P<0.01). Furthermore, no adverse effects were observed on the viability of rRMECs after QD intervention. QD effectively inhibited RNV formation, promoted neovascular maturation and remodeling, and protected retinal function by modulating the Ang/Tie2 signaling pathway. Therefore, QD may serve as a promising therapeutic option for retinal neovascular diseases.

Spermatogenesis, which is regulated by multiple cell death mechanisms, is an extremely complex process. The significance of cell death during spermatogenesis is a topic of interest because of its potential medical implications. Cuproptosis is a new mechanism of cell death discovered in recent years, and recent studies have preliminarily confirmed that cuproptosis is involved in the process of spermatogenic cell death, but its specific role in the process of spermatogenic cell death is still unclear. In this review, the mechanisms of spermatogenic cell death associated with cuproptosis and the effects of key genes of cuproptosis on spermatogenesis are discussed together with some new perspectives for the study of spermatogenic cell death.

Backgrounds Exosomes is a promising cell-free therapy for Diabetic peripheral neuropathy (DPN) that imposes long-term negative effects on patients’ finances, mental health, and quality of life. We conducted a meta-analysis to assess the therapeutic effects of exosomes (such as SCs-derived, FCs-derived, BMSCs-derived, MSCs-derived, and Plasma-derived) on DPN. Methods We searched nine databases from inception to February 2025, then two researchers independently screened studies, extracted data, and assessed the quality of included studies using SYRCLE’s tool. The outcome indicators consisted of at least one of the three key DPN endpoints (electrophysiology, behavioural assessment, and nerve structure) based on the Neurodiab guidelines. R 4.4.2 software was used to conduct all statistical analyses. Results 11 studies were identified, and the risk of bias in most studies was unclear generally. Pooled analyses demonstrated that exosome improved the nerve conduction velocity [MCV (SMD = 4.71 [2.18;7.25], P = 0.0003; I²= 91.8%), SCV (SMD = 1.07 [0.30;1.85], P = 0.0069; I²= 85.3%)], may restore IENFD [SMD = 1.46 [-0.85; 3.77], P = 0.2164; I²=88.7%], alleviated neuropathic pain [mechanical allodynia (SMD= -0.27 [-1.02;0.47], P = 0.4697; I² = 85.0%), thermal hyperalgesia (SMD= -1.48 [-2.45;-0.50], P = 0.003; I² = 88.4%)], ameliorated vascular function [blood flow perfusion in plantar (SMD = 2.84 [0.89; 4.80], P = 0.0043; I² = 74.9%), blood flow perfusion in sciatic nerves (SMD = 2.62 [0.80; 4.43], P = 0.0047; I² = 75.9%), vessel density (SMD = 2.69 [0.90; 4.49], P = 0.0032; I² = 0%)], and restored the peripheral nerve structure [sciatic nerve fiber diameter (SMD = 3.29 [1.61; 4.96], P = 0.0066; I² = 75.5%), axon diameter (SMD = 2.26 [1.64; 2.88], P < 0.0001; I² = 54.3%), myelin sheath thickness (SMD = 2.56 [1.39; 3.72], P < 0.0001; I² = 73.0%), g-ratio (SMD= -1.64 [-3.28; 0.00], P = 0.0502; I² = 34.17)]. Furthermore, after exosome therapy, the expressions of NF-200 (SMD = 2.57 [0.39; 4.75], P = 0.0210; I² = 33.0%), MBP (SMD = 2.27 [-1.49; 6.02], P = 0.1064; I² = 59.0%), and S-100β (SMD = 1.90 [0.09; 3.72], P = 0.0399; I² = 32.5%) evaluating axonal regeneration and remyelination increased significantly. Notably, high-glucose pretreatment of exosomes significantly attenuated these effects, while genetic overexpression modifications or novel dressings-mediated delivery partially counteracted this suppression. Conclusions Exosome therapy provides a novel therapeutic strategy for the benefit of neurovascular remodeling and functional recovery of DPN, especially when used in conjunction with exosome modification and novel dressings. To bridge the translational gap between preclinical and clinical studies, future research should conduct more large-scale, meticulously designed preclinical trials adhering to ARRIVE criteria before proceeding to clinical translation, to enhance translational rigor and mitigate risks associated with variability in study design.

Colorectal cancer (CRC) is a multifaceted disease influenced by genetic mutations and environmental factors, especially oxidative stress. Driver mutations are pivotal in CRC initiation and progression and alter key signaling pathways involved in cell proliferation, apoptosis, and genomic stability. Concurrently, oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a crucial role in CRC development by promoting DNA damage, lipid peroxidation, and redox signaling dysregulation. The molecular mechanisms linking driver mutations and oxidative stress pathways underscore their collective or antagonistic impact on CRC heterogeneity, therapeutic responses, and clinical outcomes. Insights into mutation-specific vulnerabilities and redox modulation offer promising avenues for targeted therapies and personalized medicine approaches in CRC treatment. Here, we discuss the intricate interplay between driver mutations and oxidative stress, highlight emerging trends, and propose future research directions to advance our understanding of CRC pathogenesis and optimize therapeutic interventions.

Background Chronic urticaria (CU), a prevalent and often debilitating allergic skin disorder, is primarily triggered by mast cell degranulation. Danggui Yinzi (DGYZ), a traditional Chinese medicine formula, has been employed to treat pruritic conditions. However, the molecular mechanisms underlying its effects in CU remain unclear. This study aimed to investigate the immunopharmacological mechanisms of DGYZ in CU, hypothesizing that it modulates immune responses through its bioactive components, which is critical for the development of novel therapeutic agents. Methods Ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (UPLC-Q-TOF–MS) was used to identify the active compounds in DGYZ. In vivo, BALB/c mouse models of DNP-IgE/DNFB-induced CU were established and grouped into Normal Control (NC), Model, various-dose DGYZ, and Loratadine groups. Post-treatment, immunopharmacological parameters were assessed, and skin tissue was collected for histopathological analysis, mast cell quantification, and immunohistochemistry to evaluate the impact on immune cells and molecules. Serum levels of inflammatory cytokines (TNF-α, IL-6) were quantified using ELISA kits. In vitro, the human mast cell line LAD2 was pretreated with key active components of DGYZ (Quercetin and Paeoniflorin) at different concentrations before mast cell degranulation was induced. Degranulation markers (β-HEX, HIS) and the expression of proteins in immune-related signaling pathways (PI3K-Akt, TLR4) were then measured. Results A total of 38 active components were identified in DGYZ. In vivo, DGYZ inhibited mast cell degranulation, blue spot reactions, and skin damage in mice. It also decreased the levels of inflammatory cytokines (TNF-α, IL-6) and suppressed the activation of associated signaling pathways. In vitro, both Quercetin and Paeoniflorin reduced mast cell degranulation and the activation of TLR4 and PI3K-Akt pathways. Conclusion This study, employing UPLC-Q-TOF–MS and both in vivo and in vitro experiments, provides a comprehensive analysis of the mechanism of DGYZ in CU. The findings indicate that DGYZ exerts therapeutic effects in CU by modulating immune responses. This research lays the foundation for a deeper understanding of its immunopharmacological mechanisms, potentially aiding the development of novel drugs and therapeutic strategies for CU management. Graphical Abstract

Background and purpose Growing evidence indicates that inflammatory cytokines may influence intervertebral disc degeneration both upstream and downstream. To further explore the upstream and downstream direct causality of inflammatory cytokines in intervertebral disc degeneration, we performed a bidirectional, two-sample Mendelian randomization (MR) study. Methods and results Five MR analysis techniques were used to explore the causal relationship, with a sensitivity analysis validating the results. We examined 91 inflammatory cytokines to assess their impact on intervertebral disc degeneration and identify upstream modulators. Three key regulators were identified: cystatin D(OR, 0.88; CI [0.78-1.00]; P = 0.04), IL-15 receptor subunit alpha (OR, 1.17; CI [1.02–1.34]; P = 0.02), and TNF-related apoptosis-inducing ligand (OR, 0.85; CI [0.75–0.98]; P = 0.02). Additionally, we examined the effects of disc degeneration on inflammatory cytokines to identify downstream effectors influencing disc degeneration. We identified four downstream effectors associated with disc degeneration: IL-13(OR 1.05, CI 1.01–1.10, P = 0.01), IL-2 (OR 0.95, CI 0.91–0.99, P = 0.02), IL-20 receptor subunit alpha (OR, 1.05; CI [1.01–1.09]; P = 0.03), and Thymic stromal lymphopoietin(OR, 1.05; CI [1.00-1.10]; P = 0.02). Conclusion This research identified a causal link between inflammatory cytokines and intervertebral disc degeneration, highlighting Cystatin D, IL-15 receptor subunit alpha, and TNF-related apoptosis-inducing ligand as key regulators, with IL-15 receptor subunit alpha possibly being the primary factor. Our hypothesis proposes that after disc degeneration, increased IL-13 and decreased IL-2 levels might slow disc degeneration and provide a protective response. Conversely, higher levels of IL-20 receptor subunit alpha and thymic stromal lymphopoietin could exacerbate inflammation and accelerate disc degeneration.

Objectives The demand for high‐quality clinical evidence supporting acupuncture remains urgent, necessitating the establishment of a suitable methodological framework to promote its generation. Methods Following internal deliberations and extensive online discussions with experts in the IDEAL Collaboration, we proposed the IDEAL‐Acu framework specifically for acupuncture, based on the surgery‐focused IDEAL model with necessary modifications to accommodate the characteristics of acupuncture. To ensure consensus on recommendations, a panel of external experts and internal research team members was convened, and any disagreements were iteratively resolved through expert review. Results This article introduces an IDEAL‐Acu framework with five stages for evaluating acupuncture outcome and improving practice to optimize treatment. The framework includes Idea (proposal of an acupuncture regime), Development (optimization or standardization of the acupuncture regime), Exploration (feasibility assessment for conducting a definitive RCT), Assessment (evaluation of effects through comparison with standard therapy or sham acupuncture), and Long‐term monitoring (examination of long‐term efficacy and safety) stages. We provide clear recommendations for each stage along with specific examples. Conclusion The framework highlights the importance of conducting studies at each stage in acupuncture evaluation process and can serve as a helpful guide for assessing its effects and promoting evidence‐based practice in acupuncture.

Background SKV-012 is a novel engineered oncolytic virus (containing the viral neurovirulence ICP34.5 gene transcribed by the Survivin promoter with an upstream genetic component of interleukin-12 (IL-12) driven by the cytomegalovirus promoter) that preferentially replicates in tumors and helps stimulate antitumor immune responses. Methods We evaluated SKV-012’s safety and efficacy in preclinical models. In a phase I trial, patients with advanced solid tumors received intratumoral injections of escalating doses of SKV-012. Primary endpoints were safety and tolerability, while secondary endpoints were antitumor response and changes in the tumor microenvironment (TME), assessed by RECIST v1.1 criteria and multiplex immunohistochemistry and single-cell transcriptome analysis. Results SKV-012-infected tumor cells secreted high levels of IL-12 and exhibited increased ICP34.5 expression. The combination of oncolytic herpesvirus and IL-12 was proven to reshape the TME by increasing the infiltration of immune cells, thereby significantly inducing immune cell-mediated cytolysis of tumor cells both in vitro and in animal models. Based on this, we then tested the safety, efficacy and immunogenicity of SKV-012 in patients with advanced solid cancers in a phase I clinical trial ( NCT06080984 ). No dose-limiting toxicities were observed, and adverse events were mild. Three patients achieved partial responses; one had stable disease and two had progressive disease. SKV-012 altered the TME, increasing CD8+ T cells, conventional dendritic cells, and programmed death-ligand 1 expression. Conclusions Intratumoral SKV-012 injections demonstrated a favorable safety profile and promising efficacy in animal models and patients with advanced cancers, thereby implicating its potential for clinical application in treatment-resistant advanced solid tumors.

The integrity of the intestinal barrier is essential for overall health. Disruption of tight junction (TJs) proteins negatively affects intestinal barrier function, leading to immune imbalances and causing a variety of pathological conditions that are closely associated with the pathogenesis of multiple diseases. Th17 and Treg cells are two distinct phenotypes of CD4⁺ T cells with opposing functions. The balance established between these two subpopulations is essential to prevent the development of disease. Emerging evidence suggests that the Th17/Treg balance is an important potential target for improving the intestinal barrier. However, there is still a lack of effective drugs for the treatment of intestinal barrier dysfunction or disorders. Polyphenols, natural compounds found in plants, have gained attention as potential therapies. Research shows that polyphenols can regulate the Th17/Treg balance by influencing key molecular pathways, such as NF‐κB, MAPK, aryl hydrocarbon receptor (AhR), and peroxisome proliferators activate receptors‐γ (PPARγ), while also improving gut microbiota. These actions help increase TJ protein levels, reduce gut permeability, and lower inflammation. Preclinical and clinical studies suggest that polyphenols may help treat conditions like inflammatory bowel disease (IBD) by restoring gut health and immune balance. In the present review, we highlight how the Th17/Treg balance affects intestinal permeability, and recent findings regarding possible effects and the molecular mechanism of polyphenols in regulating the Th17/Treg balance, to provide new potential therapeutic strategies for damaged intestinal barrier treatment preclinically and clinically.

Pulmonary fibrosis is often associated with aging, marked notably by the senescence of lung epithelial cells and the development of interstitial fibrosis. Mitophagy plays a crucial role in aging by degrading damaged mitochondria, thereby maintaining mitochondrial quality and cellular homeostasis. When mitophagy is disrupted or impaired, damaged mitochondria fail to be properly degraded by lysosomes. This results in the persistence of dysfunctional mitochondria, which can further damage cells, induce cell senescence and trigger inflammatory responses. These processes can worsen pulmonary fibrosis. Restoring proper mitophagy could be a promising strategy for managing pulmonary fibrosis and countering stress-induced premature cell senescence, potentially improving or even reversing lung function in aging lungs. This review will explore the complex relationship between cell senescence and pulmonary fibrosis, detailing the senescence characteristics in fibrotic lungs. It will also highlight recent advancements in understanding how mitophagy influences lung senescence and fibrosis and discuss potential therapeutic strategies to address mitophagy dysfunction in treating pulmonary fibrosis.

Background Arthroscopic Bankart repair can be performed via a more contemporary knotless procedure or a more traditional knotted procedure. Nonetheless, comparisons between these two techniques remain controversial. Methods Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a comprehensive search of PubMed, EMBASE, Cochrane Library, Scopus, and Web of Science was conducted. Randomized controlled trials (RCTs) and cohort studies directly comparing the knotless and knotted arthroscopic Bankart procedures were included. The primary outcomes were rates of recurrent instability and revision surgeries. Secondary outcomes encompassed number of anchors, operative time, improvements in functional scores including Rowe score and Constant-Murley score (CMS), pain level assessed by the visual analogue scale (VAS) score, range of motion (ROM), adverse events, and radiological results. Quality assessment was performed using RoB2 and MINORS tools. Meta-analysis pooled RCT data using Review Manager 5.4.1, and non-pooled outcomes from cohort studies or limited RCT data were reported separately. Results This meta-analysis included nine studies with a total of 729 patients. Pooled data from three RCTs demonstrated no significant differences between the two techniques in terms of re-dislocation (P = 0.78), recurrent anterior subluxation and positive apprehension test (P = 0.78), revision surgery (P = 0.94), number of anchors used (P = 0.26), or improvements in Rowe score (P = 0.15). For outcomes not suitable for pooling, qualitative analysis of trends indicated comparable outcomes between the groups, except a slightly reduced operative time in the knotless repair group. Adverse events were infrequently reported and occurred at similar rates in both groups. Limited radiological data from one RCT showed no significant differences in MRI parameters at the 24-month follow-up. Conclusion Both techniques demonstrate comparable clinical outcomes. The only potential advantage of the knotless technique is a possible reduction in operative time, though its clinical significance remains uncertain. Given the limitations of the evidence, these findings should be interpreted cautiously. Clinical trial number Not applicable. PROSPERO registration ID CRD42024586135.