Search Results (647)

Background: Cerebral aneurysms and aneurysmal subarachnoid hemorrhage (aSAH) may induce cardiac electrical instability through autonomic dysregulation and an exaggerated neurohumoral stress response. Electrocardiographic (ECG) abnormalities, including QT/QTc prolongation, QTc dispersion, and P-wave dispersion, are recognized markers of ventricular repolarization heterogeneity and atrial conduction abnormalities associated with arrhythmogenic risk. However, data regarding the reversibility of these electrophysiological alterations following definitive aneurysm treatment remain limited. Methods: This retrospective, single-center study included 39 patients with cerebral aneurysms who underwent microsurgical clipping between January 2025 and May 2026 and 35 age- and sex-matched healthy controls. Standard 12-lead ECGs were evaluated at baseline (preoperative) and one month after surgery in the aneurysm group. QT interval, corrected QT (QTc) interval, QTc dispersion, and P-wave dispersion were assessed using standardized methods. Baseline transthoracic echocardiographic parameters, including left ventricular ejection fraction and left atrial diameter, were evaluated to minimize potential confounding related to structural cardiac abnormalities. Between-group and within-group comparisons were performed using appropriate statistical analyses. Results: Baseline demographic and echocardiographic characteristics were comparable between the aneurysm and control groups. Patients with cerebral aneurysms demonstrated significantly higher baseline QT interval, QTc interval, QTc dispersion, and P-wave dispersion compared with healthy controls. Following microsurgical treatment, significant reductions in QT interval, QTc interval, QTc dispersion, and P-wave dispersion were observed at one month compared with preoperative values, whereas PR interval and QRS duration remained unchanged. These findings suggest a partial normalization of cardiac electrical heterogeneity after definitive aneurysm treatment. Conclusions: Cerebral aneurysms are associated with increased ventricular repolarization and atrial conduction heterogeneity, reflecting autonomic-mediated cardiac electrical instability. The significant reduction in QTc dispersion and P-wave dispersion following microsurgical treatment suggests that these electrophysiological abnormalities may be at least partially reversible after aneurysm repair. ECG-derived markers such as QTc dispersion and P-wave dispersion may represent practical and non-invasive tools for monitoring cardiac electrical instability and recovery in patients with cerebral aneurysms. Full article

Walking is not merely locomotion but a window into the nervous system, integrating cortical, subcortical, cerebellar, spinal, and peripheral networks into a unified motor behavior. Across neurological diseases—including Parkinson’s disease, atypical parkinsonism, cerebellar ataxias, stroke, multiple sclerosis, neuropathies, neuromuscular disorders, and functional gait syndromes—gait disturbances are among the most disabling clinical features, contributing to falls, loss of independence, institutionalization, and premature mortality. Traditional bedside observation remains indispensable, but it lacks the sensitivity and reproducibility needed to capture subtle, episodic, or prodromal abnormalities. Over the past decade, advances in wearable sensors, marker-based and markerless motion capture, pressure-sensitive walkways, force plates, artificial intelligence, and machine learning have positioned digital mobility outcomes as promising, ecologically valid biomarkers of neurological function. These measures can support differential diagnosis, provide prognostic information on falls and survival, and serve as sensitive endpoints in therapeutic trials. They may also detect early abnormalities, such as increased stride-to-stride variability or prolonged double-support time, before overt clinical deterioration becomes evident. Clinical applications are increasingly evident across disorders, including distinguishing Parkinson’s disease from atypical parkinsonism, quantifying treatment response in normal-pressure hydrocephalus, tracking progression in ataxia and multiple sclerosis, predicting functional decline in motor neuron disease, and guiding rehabilitation after stroke. Integration with neuroimaging, electrophysiology, and molecular biomarkers is beginning to reveal the circuits underlying variability, instability, and freezing, positioning gait as a systems-level marker of neural integrity. Nevertheless, methodological heterogeneity, limited disease-specific validation, insufficient longitudinal data, and lack of consensus on clinically meaningful parameters continue to constrain translation. Cognitive, affective, and environmental influences also remain insufficiently represented in digital frameworks, while equity, accessibility, algorithmic bias, and privacy require careful ethical governance. Reconceptualizing gait as a “sixth vital sign” reframes mobility as a multidimensional biomarker of neural and systemic health. With harmonized protocols, robust validation, multimodal integration, and appropriate ethical frameworks, gait analysis could become a cornerstone of precision neurology. Full article

Background: The click-evoked Auditory Brainstem Response (ABR) is the gold standard electrophysiological tool for assessing auditory pathway integrity in infants and young children. As normative data are inherently equipment-specific, the absence of pediatric reference values for the NeuroAudio system (Neurosoft, Ivanovo, Russia) represents a significant gap in clinical practice, given that existing normative datasets for this system are restricted to adult populations. Objective: To establish normative data for click ABR recorded with the NeuroAudio system in children under three years of age, stratified by age group according to auditory maturation patterns. Methods: A prospective, cross-sectional study was conducted at the Electrophysiology Laboratory of the Department of Speech Therapy, Paulista School of Medicine, Federal University of São Paulo (UNIFESP/EPM), under the approval of the Research Ethics Committee (protocol 7.939.564). A total of 203 children (121 males, 82 females; age range: 2 weeks to 36 months) with confirmed normal peripheral auditory function were included. Click stimuli (0.1 ms, rarefaction polarity) were delivered monaurally via ER-3A insert earphones at 80 dB nHL and a repetition rate of 19.3/s. Two average runs of 2000 artifact-free sweeps were recorded per ear. Absolute latencies of waves I, III, and V, interpeak intervals I–III, III–V, and I–V, and amplitudes of waves I and V were analyzed. Results: Statistical modeling supported the consolidation of 12 initial age bins into three clinically and statistically validated categories: 0–3, 4–12, and 13–36 months. Wave I latency remained stable across age groups, whereas waves III and V and all interpeak intervals showed progressive shortening with increasing age. Wave V amplitude increased progressively with age, while wave I amplitude remained unchanged. Females presented shorter latencies than males for waves III and V and for all interpeak intervals. The right ear exhibited a shorter III–V interpeak interval than the left ear, with a significant ear × age interaction indicating that this asymmetry is modulated during early maturation. Age, sex, and ear-stratified normative values (two SD and three SD reference limits) are reported. Conclusion: This study provides the first pediatric normative dataset for click-evoked ABR acquired with the NeuroAudio system in children under three years of age. The proposed three age stratifications, together with sex- and ear-specific reference values for the III–V interpeak interval, offer a clinically actionable framework for the accurate interpretation of pediatric ABR recordings and for the early identification of auditory pathway abnormalities. Full article

Background and Clinical Significance: Biallelic pathogenic variants in the PCARE gene (photoreceptor cilium actin regulator), also known as C2orf71 (chromosome 2 open reading frame 71), are typically associated with retinitis pigmentosa type 54 (RP54) and, less frequently, with cone–rod dystrophy (CORD23). Case Presentation: A 52-year-old man presented with an eight-year history of progressive visual loss, without photophobia or nyctalopia. He underwent a comprehensive ophthalmological evaluation, including multimodal retinal imaging, automated perimetry, and full electrophysiological testing, in accordance with International Society for Clinical Electrophysiology of Vision (ISCEV)’s standards. Genetic testing was performed using next-generation sequencing (NGS) with an inherited retinal dystrophy gene panel, and findings were confirmed by Sanger sequencing. Clinical examination revealed bilateral macular atrophy with minimal foveal sparing and a central scotoma. Optical coherence tomography (OCT) showed disruption of the outer retinal layers and retinal pigment epithelium (RPE) abnormalities. Fundus autofluorescence (FAF) demonstrated central hypoautofluorescence surrounded by a hyperautofluorescent ring. Electrophysiological testing revealed severely reduced rod- and cone- mediated responses on full-field electroretinography (ERG), absent pattern ERG responses, and markedly reduced multifocal ERG responses, indicating widespread retinal dysfunction with significant macular involvement. Genetic analysis identified a homozygous pathogenic nonsense variant in PCARE [c.3289C>T; p.(Gln1097*)], confirming the diagnosis of an autosomal recessive inherited retinal dystrophy. Conclusions: Biallelic PCARE variants can cause late-onset severe retinal dystrophy, with predominant macular involvement and cone–rod dysfunction. Given its phenotypic overlap with other inherited retinal diseases, accurate diagnosis requires the integration of multimodal retinal imaging, electrophysiological testing, and comprehensive genetic analysis. Full article

Shear wave elastography (SWE) is an increasingly investigated ultrasound-based technique in musculoskeletal imaging that provides quantitative information on tissue stiffness and biomechanical properties. This narrative review aims to summarize the basic principles, technical considerations, current clinical applications, limitations, and future perspectives of SWE in musculoskeletal imaging. Unlike conventional grayscale and Doppler ultrasonography, which mainly assess morphology and vascularity, SWE may provide additional functional information in major musculoskeletal tissues, including tendons and ligaments, skeletal muscles, peripheral nerves, fibrocartilaginous structures, plantar fascia, and selected soft tissue lesions. Current evidence suggests potential roles for SWE in detecting early biomechanical alterations, assessing disease severity, differentiating symptomatic from asymptomatic tissues, and monitoring response to treatment or rehabilitation. However, musculoskeletal tissues are anisotropic, viscoelastic, and position-dependent; as a result, SWE measurements are influenced by acquisition-related factors, tissue biomechanics, positioning and loading conditions, region of interest (ROI) placement, tissue depth, and device-related variability. For this reason, SWE findings should not be interpreted as standalone diagnostic criteria but should be considered together with clinical findings, conventional ultrasonography, MRI, electrophysiology, histopathology, and patient-centered outcomes when appropriate. This review highlights the need for tissue-specific measurement protocols, standardized reporting, normative reference data, inter-vendor harmonization, and longitudinal validation against clinically meaningful outcomes before SWE can be more reliably integrated into routine musculoskeletal imaging and rehabilitation practice. Full article

Objective: Sodium–glucose cotransporter 2 (SGLT2) inhibitors, particularly empagliflozin, have attracted considerable attention because of their cardiovascular benefits beyond glycemic control. However, the interaction between empagliflozin and exercise-induced physiological cardiac remodeling in healthy individuals remains insufficiently understood. This study investigated the effects of different swimming exercise protocols (anaerobic, aerobic, and endurance), administered alone or in combination with empagliflozin, on cardiac structure and electrophysiology. Methods: Thirty-six male Sprague–Dawley rats were randomly assigned to six groups (n = 6 per group): anaerobic (An), aerobic (Ae), endurance (En), and the corresponding exercise groups combined with empagliflozin (An + Empa, Ae + Empa, and En + Empa). Empagliflozin was administered by oral gavage at a dose of 15 mg/kg/day for 30 days. Transthoracic echocardiography, electrocardiography (ECG), and gastrocnemius electromyography were performed at baseline and at the end of the study to assess cardiac remodeling, heart rate, and neuromuscular function. The study was carried out over a 30-day intervention period following ethics committee approval on 24 July 2024. Results: No significant between-group differences were observed in echocardiographic parameters before the intervention. On day 30, significant differences were identified among the groups in interventricular septal thickness at end-diastole (IVSd) (p = 0.027), left ventricular internal diameter at end-diastole (LVIDd) (p = 0.009), and end-diastolic volume (EDV) (p = 0.014). Bonferroni-corrected post hoc analysis showed that the aerobic exercise plus empagliflozin group differed from several exercise-only groups, particularly in parameters related to ventricular size and filling volume, including LVIDd and EDV (p < 0.008). On day 30, electrocardiographic repolarization-related parameters, including QT, QTc, JT, and Tpeak–Tend intervals, also differed significantly among the groups (all p < 0.05). In post hoc analysis, the anaerobic exercise group showed significant differences in QT and JT intervals compared with the aerobic and endurance groups (p < 0.008). In the anaerobic protocol, empagliflozin was associated with a reduction in heart rate compared with the corresponding control group (p = 0.019). No significant between-group differences were observed in EMG findings. Conclusions: Different exercise protocols induce distinct patterns of adaptation in cardiac structure and electrophysiology in healthy rats. Empagliflozin (15 mg/kg/day) may modulate exercise-induced cardiac responses in a modality-dependent manner; the most pronounced echocardiographic effects were observed in the aerobic protocol, whereas the effect on heart rate was observed in the anaerobic protocol. These findings highlight the need for longer-term and mechanistic studies to further clarify the effects of SGLT2 inhibitors on physiological cardiac remodeling. Full article

Seleniferous tea seedlings from Enshi, China, face cadmium (Cd) contamination risks due to the co-occurrence of selenium and cadmium in local soils, posing food safety concerns. While Astragalus sinicus-modified substrates are commonly applied for cadmium remediation, the performance of different monitoring techniques remains inadequately evaluated. This study compared four monitoring methods—growth traits, photosynthesis, chemical Cd removal rate, and plant electrophysiological parameters—in a pot experiment under cadmium stress (10 mg/kg Cd²⁺). Two tea varieties, Longjing 43 (Camellia sinensis ‘Longjing 43’. LJ 43) and Yulu 1 (Camellia sinensis ‘Yulu 43’. YL 1), were treated with four modified substrates (M1–M4). Specifically, compared to the control (M1), LM3 increased metabolic activity (MA), electrical impedance (EGC), and electrochemical response (ECR) by 140.27%, 122.5%, and 124.41%, respectively. These increases were significantly greater than those observed for the conventional metrics: 52.70% in total biomass (TB), 109.31% in photosynthetic rate (Pn), and 64.15% in chemical Cd removal (R_Cd). Similarly, in the YM4 treatment, MA and EGC increased by 214.91% and 178.66%, respectively, which also significantly exceeded the increments in TB (48.74%), Pn (116.19%), and R_Cd (75.26%). Among the electrophysiological parameters, MA proved to be the most sensitive indicator, showing a strong correlation with Cd removal capacity. In conclusion, plant electrophysiology enabled real-time, in situ monitoring of cadmium remediation efficiency, offering a novel technological pathway to ensure the safety of seleniferous tea seedlings and advance precision agriculture. Full article

Orthodontic pain, a fundamental biological response to mechanically induced tooth movement, is primarily associated with sterile inflammation and neurogenic processes within the periodontal ligament (PDL). Although photobiomodulation therapy (PBMT) has been widely investigated as a nonpharmacological approach for pain attenuation, its mechanisms of action remain incompletely understood, and current interpretations are often limited to peripheral anti-inflammatory effects. This review re-examines the biological basis of orthodontic pain by integrating evidence derived predominantly from in vitro and in vivo experimental studies. Particular emphasis is placed on neurogenic inflammation, neuropeptide regulation, and neuron–glia interactions along the trigeminal nociceptive pathway. PBMT can reduce periodontal inflammatory/neuropeptide-related markers and pain-related behaviors in selected models; however, evidence for direct central neuron–glia modulation remains largely marker-based and parameter-dependent. Direct functional validation of trigeminal circuit modulation (e.g., electrophysiological recordings or calcium imaging) remains limited in orthodontic pain models; thus, the proposed neuroimmune mechanisms should be interpreted as testable hypotheses for future work. By synthesizing mechanistic insights across multiple biological levels, this review proposes a broader framework for understanding PBMT-mediated pain modulation extending beyond conventional peripheral models. These perspectives may help clarify inconsistencies in the reported outcomes and provide a rationale for future hypothesis-driven experimental and translational research. Full article

The ability to distinguish speakers based on speech signals is a fundamental human ability essential for social communication, yet the neural mechanisms underlying this process remain poorly understood. The present study investigated the temporal dynamics of neural activity during speaker discrimination using event-related potentials (ERPs). Twenty-four native Mandarin speakers completed two tasks: an oddball session, in which participants passively listened to speech stimuli from standard and deviant speakers, and a voice line-up session, in which participants explicitly judged whether two consecutively presented speech stimuli were produced by the same or different speakers. In the oddball session, deviant stimuli elicited robust mismatch negativity (MMN) and P3a components compared to standard stimuli, indicating pre-attentive detection of speaker changes. In the voice line-up session, the different-speaker condition elicited more negative N1 and N400 amplitudes and more positive P2 amplitudes than the same-speaker condition, suggesting that speaker discrimination engages both early sensory processing and later cognitive integration. No significant differences were observed between the P300 and P600 components. These findings reveal distinct neural signatures associated with speaker-related processing across multiple temporal stages, with the MMN and P3a reflecting automatic detection of speaker-related acoustic changes, and the N1, P2, and N400 reflecting explicit speaker discrimination processes. While the present paradigm cannot fully isolate identity-level representations from low-level acoustic discrimination, the results provide novel ERP evidence on the temporal architecture engaged when listeners process speaker-specific information, contributing to a deeper understanding of speaker-related processing in the broader context of speaker identification research. Full article

Motoneurons are under strong pressure to maintain stable motor output throughout an individual life, through homeostatic regulation of their electrical properties. Dysregulated spinal motoneuron excitability has long been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Recent work in SOD1^G93A mice suggests that the homeostatic response of motoneurons becomes dysregulated as cellular processes are disrupted by the disease, causing fluctuations in motoneuron electrical properties. Yet, few studies directly test whether ALS motoneurons respond differently than wild-type motoneurons to a common chronic perturbation. Here, we used in vivo electrophysiology to test whether motoneurons from pre-symptomatic SOD1^G93A mice modulate excitability differently than wild-type motoneurons in response to the same homeostatic perturbation: chronic inhibition exerted by the benzodiazepine diazepam. Using linear mixed-effects statistical models, we assessed whether diazepam treatment differentially modulated passive properties, firing behavior, spike properties, and/or synaptic inputs in SOD1^G93A versus wild-type motoneurons. We identified a significant genotype × treatment interaction effect selectively for properties related to passive membrane integration and spike initiation, including membrane time constant, peak input resistance, and recruitment current. In contrast, firing gain, spike waveform characteristics, and synaptic inputs were largely unaffected. These findings indicate that sustained inhibitory perturbation selectively triggered overactive intrinsic compensatory mechanisms in SOD1^G93A motoneurons rather than inducing widespread changes in firing or synaptic transmission. Together, our results provide direct evidence for over-active homeostatic control of motoneuron excitability and support a view of motoneuron dysfunction in ALS as a problem of altered feedback regulation rather than simply hyper- or hypo-excitability. Full article

Spinal cord stimulation (SCS) is an established therapy for chronic pain, yet treatment response remains highly variable and patient selection largely empirical. The identification of biomarkers with the potential to predict and monitor therapeutic response is therefore critical for advancing toward precision neuromodulation. This study provides a structured narrative synthesis of current evidence on biomarkers in SCS, focusing on their predictive and monitoring roles and their translational potential. Available studies were analysed across electrophysiological, neuroimaging, autonomic, and molecular domains and conceptually organized into predictive biomarkers—reflecting baseline biological states associated with treatment susceptibility—and monitoring biomarkers, capturing physiological and molecular adaptations following stimulation. Among predictive approaches, intraoperative electroencephalography (EEG) and resting-state functional magnetic resonance imaging (rs-fMRI) have shown promising but exploratory discriminative performance. However, EEG findings are derived from intraoperative settings, limiting their applicability to pre-implantation patient selection. In contrast, monitoring biomarkers—including heart rate variability, metabolic imaging, and immunological parameters—provide objective measures of treatment-induced changes but do not currently support predictive use. Molecular and genomic biomarkers, while mechanistically informative, remain exploratory and lack validated clinical utility. A central limitation of the field is the fragmentation of biomarker research, with most studies evaluating single modalities in isolation. To address this gap, we propose a translational framework integrating predictive and monitoring biomarkers through a two-stage model combining baseline stratification with longitudinal response assessment. Although biomarker research in SCS is rapidly evolving, its clinical application remains limited. The development of multimodal, validated biomarker strategies may support improved patient selection and more objective evaluation of treatment response, enabling a transition toward mechanism-based neuromodulation. Full article

Cardiac arrhythmias are increasingly recognized as dynamic clinical phenotypes arising from the interplay between myocardial substrate, systemic biology, and modifiable exposures rather than as isolated disorders of cardiac electrophysiology. Advances in the field have broadened the conceptual framework of arrhythmia medicine to include structural remodeling, inflammation, autonomic dysfunction, metabolic perturbation, endothelial injury, and aging-related vulnerability as central determinants of arrhythmic risk, progression, and treatment response. In parallel, diagnostic paradigms are evolving from rhythm classification alone toward multidimensional phenotyping that integrates clinical, physiological, and imaging-based markers to identify susceptibility earlier and with greater precision. These developments are also reshaping therapeutic strategy, supporting a shift from uniform treatment algorithms toward individualized care in which rhythm control, surveillance, risk-factor modification, anticoagulation, and antiarrhythmic drug selection are aligned with the underlying biological context. This more integrated view positions arrhythmias not simply as electrical events to be suppressed, but as manifestations of broader cardiovascular and systemic disease processes that require mechanistically informed and phenotype-directed management. Full article

Optogenetic gene therapy-based treatment offers a unique approach to bypass dysfunctional or degenerated photoreceptors in retinal degenerative disorders. Ambient light-activatable multi-characteristic opsin (MCO) targeted to bipolar cells of the retina has demonstrated partial vision restoration in animal models of retinitis pigmentosa (RP). Here, we describe the potential therapeutic efficacy of intravitreally delivered AAV-carried MCO-010 in a mouse model of Stargardt disease. MCO-010 treatment led to significantly improved behavioral outcomes in the visually guided radial arm water maze. Furthermore, longitudinal optical coherence tomographic imaging showed that the MCO-010 treatment led to no notable change in the retina thickness. Furthermore, the MCO-010-treated mice exhibited higher electrophysiological responses compared to the control group. Together, these findings demonstrate potential vision-restoring and disease-modifying aspects of ambient light-activatable intravitreal MCO-010 therapy. Full article

Introduction: Schizophrenia is characterised by distributed abnormalities in electrophysiological dynamics and large-scale brain networks, yet unimodal EEG or MRI alone cannot fully explain how fast neural computations relate to spatially organised circuit dysfunction. Multimodal EEG–MRI approaches offer a bridge across temporal and anatomical scales by explicitly modelling cross-modal coupling. Methods: Following PRISMA 2020 guidance, we conducted a systematic, mechanistic review of human studies (adults ≥ 18 years) comparing schizophrenia-spectrum groups with healthy controls using EEG combined with at least one MRI modality (fMRI, structural MRI, and/or diffusion MRI) and explicit EEG–MRI integration (e.g., EEG-informed fMRI, joint ICA, mCCA/MCCA, coupled matrix–tensor factorisation, DCM-based fusion). Searches were performed in PubMed/MEDLINE, Embase, Web of Science, Scopus, PsycINFO, IEEE Xplore, ResearchGate, and Google Scholar for January 2000–December 2025, supplemented by citation tracking. Risk of bias was assessed with ROBINS-I, and due to heterogeneity, results were synthesised narratively by integration of families. Results: From 148 records, 23 studies met the inclusion criteria. Studies used mainly simultaneous EEG–fMRI at 3T and spanned resting-state designs and task paradigms dominated by auditory processing (oddball, MMN/N100–P200, ASSR/aeGBR), with additional work in affective context, working memory, semantic processing (N400), sensory gating, and pharmacologic challenge. Across tasks, the most reproducible multimodal signature was disrupted coupling between electrophysiological markers and the recruitment of large-scale networks, rather than isolated changes in EEG or fMRI metrics. Target detection/oddball paradigms converged on reduced late ERP responses (especially P300, sometimes N2) alongside reduced expression or loss of coupling to salience/ventral attention and control circuitry (including ACC/anterior insula/TPJ). Resting-state studies most consistently indicated altered “coupling rules” (frequency specificity, timing/lag structure, and directionality), including abnormalities detectable even when unimodal summaries were weak. Extended multimodal studies (adding sMRI/DTI and/or classification) suggested that combining modalities can improve discrimination, though performance was sensitive to sample size, demographic imbalance, and feature-selection/validation choices. Conclusions: Multimodal EEG–MRI studies support schizophrenia as a disorder involving persistent structural and circuit-level abnormalities whose functional expression varies dynamically across cognitive states and task demands. Future progress will depend on harmonised acquisition/artefact-control practices for simultaneous EEG–fMRI, larger and more diverse samples (including early/CHR and longitudinal designs), and cross-site replication of mechanistically interpretable coupling biomarkers. Full article

Sports injuries, especially musculoskeletal and neurological types from strenuous exercise, are a global public health challenge. Characterized by a high incidence and slow recovery, these injuries differ from typical trauma, often resulting in severe mechanical transmission loss and an imbalanced immune microenvironment. Consequently, standard interventions struggle to achieve true tissue regeneration. Gelatin, a collagen-derived biomaterial, offers RGD-mediated cell adhesion, MMP-responsive degradation, and high modifiability. These qualities make it an excellent foundation for biomimetic repair scaffolds. This paper reviews the design principles and recent advances in gelatin-based multifunctional hydrogels in sports medicine. First, we analyse their structure and engineering advantages. Next, we summarise strategies and mechanisms for modules like conductivity, antibacterial activity, self-healing, stimulus responsiveness, and tissue adhesion. The review links these modules to types of injuries: bone or cartilage, tendon or ligament, skeletal muscle, spinal cord, and peripheral nerve. It clarifies their clinical and translational value in remodelling immune microenvironments, regulating electrophysiology, promoting interfacial regeneration, and restoring motor function. This review provides focused insights from materials science and sports rehabilitation to advance precision treatments for sports injuries. Full article