Search Results (237)

Intelligent-assisted assessment of pilot flight training ability is a method of automating the evaluation of pilots’ flight skills using artificial intelligence. Currently, using AI to assist or replace human instructors in flight skill assessment has become a mainstream research direction in the field of intelligent aviation. Existing flight skill assessment methods suffer from limitations in data types and insufficient assessment accuracy. To address these issues, we evaluate and predict pilot performance in simulated flight missions based on physiological signals. Following the “OODA loop” theory, we established a multimodal dataset including pilot eye movement, electroencephalogram (EEG), electrocardiogram (ECG), electrodermal signaling (EDS), heart rate, respiration, and flight attitude data. This dataset records changes in physiological rhythms and flight behaviors during pilots’ flight training at different difficulty levels. To enhance the signal-to-noise ratio, we propose an enhanced wavelet fuzzy thresholding denoising algorithm utilizing LSTM optimization. We address the problem of isolated features across different time frames in multimodal data modeling by introducing a multi-feature fusion algorithm based on STFT. Furthermore, by combining a high-efficiency sub-attention mechanism with a Transformer network, we construct a multi-classification network for intelligent-assisted assessment of pilot flight training ability, further improving the output accuracy of each category. Experiments show that our designed algorithm can achieve a classification accuracy of up to 85% on the dataset (5-fold cross-validation), which meets the requirements for auxiliary assessment of flight capabilities. Full article

Background: Cardiorenal syndrome (CRS) represents a complex clinical entity characterized by the bidirectional dysfunction of the heart and kidneys. Despite advances in pharmacological therapy, CRS remains associated with high morbidity and mortality. Pathophysiological drivers, including oxidative stress, chronic inflammation, and mitochondrial derangements, create a self-perpetuating cycle of organ damage that necessitates multitarget therapeutic approaches. Objective: This review synthesizes current preclinical evidence regarding the protective roles of plant-derived polyphenols—specifically bergamot, curcumin, quercetin, catechins, and resveratrol—in mitigating the cardiorenal continuum. Methods: An analysis of recent literature was conducted, focusing on the molecular mechanisms by which these bioactives modulate redox balance, inflammatory signaling, and mitochondrial homeostasis in experimental models of CRS. Results: Polyphenols act at the crossroads of several stress-response pathways. Key mechanisms include the activation of the Nrf2/HO-1 axis to enhance endogenous antioxidant defenses, the suppression of the NLRP3 inflammasome to attenuate systemic “inflammaging”, and the preservation of mitochondrial quality through SIRT1/PINK1/Parkin-mediated mitophagy. Furthermore, emerging evidence highlights the role of polyphenols in modulating the gut-kidney-heart axis by reducing microbiota-derived uremic toxins. Conclusions: Preclinical data suggest that polyphenols are potent multifunctional agents capable of breaking the feedback loops of cardiorenal injury. While bioavailability remains a significant translational challenge, novel nano-delivery systems and synthetic analogs offer promising strategies for clinical application. Integrating these bioactives into CRS management could provide a decisive adjunctive strategy to improve metabolic homeostasis and prevent end-stage organ failure. Full article

Background: Left ventriculo-arterial coupling (VAC) integrates the interaction between left ventricular contractility and the arterial system, representing a key determinant of cardiovascular efficiency. In rapidly changing hemodynamic states such as septic or cardiogenic shock, conventional indices of pressure or flow alone may be misleading. VAC provides a unified physiological framework to assess global cardiovascular performance and guide therapy. Objective: To review the physiological foundations, bedside assessment, and therapeutic applications of VAC in critically ill patients with rapidly fluctuating circulatory conditions. Methods and Content: The article revisits the underlying principles of VAC, expressed as the ratio between arterial elastance (Ea) and end-systolic elastance (Ees), and discusses their derivation from the pressure–volume relationship. Practical echocardiographic methods for bedside estimation, including the non-invasive single-beat approach, are outlined with illustrative figures. The review further examines how VAC patterns evolve in sepsis, cardiogenic shock, and heart failure and how this integrative index clarifies paradoxical responses to vasoactive and inotropic therapies. Specific therapeutic phenotypes are proposed according to Ea/Ees profiles, providing a structured approach to optimise coupling and restore circulatory efficiency. Summary: VAC offers a physiology-based perspective on cardiovascular performance, enabling clinicians to interpret complex hemodynamic changes beyond traditional measures of ejection fraction or mean arterial pressure. Its dynamic tracking may refine the assessment of therapeutic trajectories and improve bedside decision-making. Conclusions: By integrating ventricular and arterial function into a single measure, VAC bridges cardiovascular physiology and clinical practice. Its incorporation into routine critical care monitoring could enhance individualised hemodynamic management and serve as a foundation for future outcome-driven studies. Methodology: This narrative review was conducted using a structured literature search to ensure comprehensive coverage of contemporary evidence regarding ventriculo-arterial coupling (VAC) in critical care and shock states. A systematic search of PubMed/MEDLINE, Embase, and Scopus databases was performed from database inception through October 2025. The following key search terms were used: “ventriculo-arterial coupling”; “arterial elastance”; “end-systolic elastance”; “Ea/Ees”; “pressure–volume loops”; “septic shock”; “cardiogenic shock”; “critical care echocardiography”; “point-of-care ultrasound”; “mechanical circulatory support”. Reference lists of relevant articles, review papers, and consensus documents were also manually screened to identify additional pertinent studies. Only English-language publications were included. Both seminal foundational studies and recent contemporary investigations were reviewed to provide historical context and up-to-date clinical applicability. Full article

Background: Elderly patients with heart failure with reduced ejection fraction (HFrEF) who experience worsening heart failure (wHF) remain at high residual risk despite optimal medical therapy (OMT), and data on cognitive function and comprehensive geriatric assessment (CGA) in this setting are lacking. This study evaluated the association between 12-month treatment with vericiguat and changes in cardiac, functional and geriatric parameters in elderly patients with recent wHF. Methods and results: In this single-center prospective observational study, 55 patients (45 men, mean age 76.4 ± 5.1 years) with HFrEF on OMT and a recent episode of wHF were treated with vericiguat and followed for 12 months. Clinical assessment, CGA and echocardiography including speckle-tracking were performed at baseline, 6, and 12 months. At 12 months, the mean vericiguat dose was 5.5 ± 2.9 mg/day. NT-proBNP levels decreased from 980 (467–2106) to 654 (274–1762) pg/mL (p < 0.0001), while left ventricular ejection fraction increased from 36.8 ± 3.1% to 43.4 ± 5.7% (p < 0.0001). Global longitudinal strain improved from −9.2 ± 1.7% to −11.5 ± 2.1% (p = 0.008), with parallel improvements in right ventricular function and pulmonary pressures. Cognitive performance improved (MMSE 25.1 ± 1.7 to 26.2 ± 2.1 points, p < 0.0001), as did depressive symptoms (GDS 7.8 ± 2.0 to 5.4 ± 1.6 points, p < 0.0001), physical performance (SPPB 6.7 ± 1.1 to 8.4 ± 0.9 points, p < 0.0001), and gait speed (0.70 ± 0.10 to 0.83 ± 0.06 m/s, p < 0.0001). Conley score decreased from 5.2 ± 2.3 to 2.4 ± 1.8 points (p < 0.0001), suggesting a lower risk of falls. Loop diuretic and MRA use were significantly reduced during follow-up. Conclusions: In this elderly HFrEF cohort with recent wHF on contemporary OMT, 12-month treatment with vericiguat was associated with consistent improvements in cardiac structure and function, biomarkers, and multidimensional geriatric status. These hypothesis-generating findings support the integration of CGA into future controlled studies of vericiguat in frail older patients with HFrEF. Given the observational design and lack of a control group, causal inference is not possible. Full article

The natriuretic peptides A and B, encoded by NPPA and NPPB, respectively, have complementary and redundant functions in cardiovascular homeostasis. To establish their coordinated roles, we analyzed the cardiac phenotype of a mouse line in which the Nppa–Nppb cluster was deleted from the genome. At 8 weeks of age, Nppa–Nppb^−/− mice (HOM) had significantly larger hearts and cardiomyocytic hypertrophy compared to wild-type and heterozygous mice. Electrocardiogram comparisons showed QRS prolongation in HOM mice. Hypertrophy was confirmed by echocardiography, which further indicated preservation of left ventricular systolic function. Bulk-transcriptomic analysis revealed moderate changes in gene expression of the left ventricle. Genes involved in fatty acid metabolism, ion handling and conductivity, including genes marking the ventricular conduction system, were down-regulated. Spatial transcriptomic analysis revealed the greatest changes in gene expression in the subendocardial wall, where the ventricular conduction system is located. Tbx5, the encoding dosage-sensitive T-box transcription factor Tbx5 that is essential for the expression of ventricular conduction system genes and for Nppa and Nppb, was down-regulated in the ventricles of HOM mice, indicating that a positive feedback loop normally maintains Tbx5 expression. We conclude that homozygous Nppa–Nppb deficiency in mice causes cardiac hypertrophy, including a likely perturbation of the ventricular conduction system. Full article

Background: Brugada syndrome (BrS) is a genetic cardiac arrhythmia disorder inherited in an autosomal dominant manner, characterized by ST-segment elevation in the right precordial leads (V1–V3) on electrocardiograms (ECGs). This syndrome predominantly affects young individuals with structurally normal hearts and significantly increases the risk of ventricular arrhythmias and sudden cardiac death (SCD). The most common genotype found among BrS patients is caused by variants in the SCN5A gene, which lead to a loss of function of the cardiac sodium channel Nav1.5 by different mechanisms. Methods: Plasmids containing SCN5A were constructed using PCR and site-directed mutagenesis to create the D372H variant. HEK293 cells were cultured and transfected with the WT, D372H, or a combination of both plasmids. Patch-clamp recordings assessed sodium current characteristics. Confocal microscopy visualized channel localization. Quantitative RT-PCR was used to analyze mRNA expression levels, while Western blot evaluated protein expression using specific antibodies. Results: In HEK293 cells expressing the D372H mutant, functional assays revealed a near-complete loss of sodium currents. Co-transfection of WT and D372H plasmids resulted in a significant reduction in current density compared with WT alone, while activation, inactivation, and recovery kinetics were unaffected. In addition, both the mutant protein and protein expressed in co-transfected cells exhibited reduced fluorescence intensity, indicating decreased expression levels. These findings were further supported by Western blot and RT-qPCR analyses. Conclusions: In summary, our findings indicate that the D372H variant produces a marked reduction in Nav1.5 function through reduced sodium current density and decreased channel expression. Given its critical position within the DI-pore loop, this defect is expected to markedly diminish the inward sodium current necessary for normal depolarization. Such impaired excitability—particularly relevant in the right ventricular outflow tract—may accentuate regional differences in repolarization and create conditions that favor reentrant activity. These findings provide mechanistic insights into how the p.D372H variant alters Nav1.5 channel function in vitro and offer functional evidence that may assist in interpreting its potential relevance to Brugada syndrome. Full article

Background/Objectives: Implantable loop recorders (ILRs) enable long-term electrocadiographic monitoring and are established diagnostic tools for syncope and atrial fibrillation (AF). However, their diagnostic yield and therapeutic impact in other clinical settings remain less well defined. We aimed to evaluate the diagnostic yield and clinical impact of ILR implantation across contemporary clinical indications. Methods: In this retrospective single-center study, 388 patients who underwent ILR implantation between 2011 and 2018 were included. Indications were categorized into seven groups: unexplained syncope, presyncope, cryptogenic stroke or transient ischemic attack (TIA), AF detection, AF recurrence after atrial flutter (AFL) ablation, risk stratification in structural or inherited heart disease, and palpitations. Results: Among 388 patients (median age 63 [51.8–71.8] years, 57.5% male; median follow-up 17.0 [IQR 6.4–32.4] months), ILRs were most frequently implanted for syncope (44.6%), AF (20.4%), and stroke/TIA (12.9%). ILR-detected arrhythmias occurred in 241 patients (62.1%), with the highest detection rates in AF (83.5%) and AFL (73.7%). Indication-fulfilling diagnoses were established in 155 patients (39.9%), most frequently in AF (73.4%) and AFL (71.1%), after a median of 4.4 months (IQR 2.4–12.5). Nearly three quarters (72.9%) of diagnoses were made within the first year. ILR findings prompted therapeutic interventions in 156 patients (40.2%), including pacemaker implantation in syncope and rhythm- or anticoagulation-based therapies in AF. AF and AFL independently predicted higher diagnostic yield, while diagnostic yield and AF history predicted ILR-triggered therapy. AF, AFL, stroke/TIA, and AF history were associated with shorter time to first arrhythmia detection. Arrhythmia-free survival differed significantly across indication groups (p < 0.0001) and was lowest in AF and AFL, which demonstrated the highest cumulative incidence of indication-fulfilling arrhythmias. Conclusions: ILRs provide substantial diagnostic and therapeutic value across a broad range of indications. Beyond established uses in syncope and AF, clinically relevant yields were observed in presyncope, risk stratification, and AFL post-ablation, supporting broader consideration of ILRs and optimized patient selection. Full article

The recovery of water and other resources from urban water systems (UWSs) has long been practiced in many Mediterranean countries, but remains relatively unexplored in Croatia. In this study, the sustainable circulation processes of water, nutrients, energy, and their components in UWSs in coastal tourist areas are analyzed in order to strengthen urban systems and environmental sustainability. Dissipative structure theory is used to critically analyze the complexity and sustainability of UWSs, urban systems, and circular economy frameworks. This study is based on conceptual analysis and knowledge (experience), and the sustainability of a circular urban water system is assessed based on circular thermodynamics. This study examines the core concepts of circular urban water systems as a local resource for nutrients, water, and energy, integrating approaches that strengthen resource recovery concepts. Systemic urban climate adaptation and circular urban systems have been adopted as interrelated strategies for resilient cities, focusing on closing resource loops while building resilience to climate impacts through whole-system approaches. This framework moves beyond single solutions, connecting urban planning, energy, water, waste, and social factors to incorporate green and low-carbon developments into cities. It was established that the principle of integrated resource management lies at the heart of effective water, energy, and nutrient management in coastal urban areas, which treats entire urban life support systems as an interconnected system. Such systems increase the efficiency percentages of water, nutrient, and energy recovery while minimizing sludge volume and system entropy, thus supporting the tourism economy and low-carbon development. Full article

Background/Objectives: Dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) are common cardiomyopathies associated with heart failure. Electrocardiogram (ECG) screening before an echocardiogram could help streamline diagnosis, particularly in rural areas. Prior ECG–machine learning (ML) studies do not use open-source data when studying cardiomyopathy, and very few proprietary studies directly compare HCM and DCM or address ECG differences within obstructive (HOCM) and non-obstructive HCM (HNCM). Methods: Standard and vectorcardiogram-derived (VCG) ECG features were extracted from the MIMIC-IV-ECG database. The final cohort comprised 599 patients (HCM = 208 [HOCM = 99, HNCM = 53, unknown = 56]; DCM = 391 [ischemic cardiomyopathy with left ventricular dilation = 250, non-ischemic = 141]). Logistic regression (LR) and extreme gradient boosting (XGBoost) with five-fold cross-validation separated HCM from ischemic cardiomyopathy with left ventricular dilation (DCM-I) and non-ischemic DCM (DCM-NI), and HOCM from HNCM. Results: Using the area under the receiver-operating-characteristic curve (AUC-ROC) as the performance metric, LR achieved high discrimination of HCM from DCM-I (0.92) and DCM-NI (0.90). However, differentiating HOCM from HNCM proved more difficult (XGBoost = 0.81; LR = 0.75). Both DCM subtypes (especially ischemic) showed lower QRS amplitudes and right-posterior ventricular gradient orientation; HCM displayed higher amplitudes and larger, more complex T-loops. Within HCM, HOCM had stronger leftward electrical activity and more dipolar to non-dipolar QRS energy after singular value decomposition. Conclusions: Using only open-access data, we demonstrate an interpretable ECG-based pipeline that discriminates cardiomyopathy and highlights distinct features. While detecting obstruction remains difficult, ECG features provide measurable separation, supporting possible diagnostic screening and offering a reproducible framework for future studies. Full article

Background/Objectives: Cardiac resynchronization therapy (CRT) is a cornerstone treatment for heart failure with reduced ejection fraction (HFrEF), yet many patients remain symptomatic despite long-term electrical optimization. Although sacubitril/valsartan (ARNI) is central to guideline-directed medical therapy (GDMT), data on its late initiation in patients with chronic CRT are scarce. This study evaluated the impact of delayed ARNI initiation on clinical status, functional capacity, and cardiac remodelling in a real-world CRT population. Methods: We performed a single-centre, retrospective observational study including 76 HFrEF patients with chronic CRT who started ARNI between 2022 and late 2024. Patients underwent standardized assessment at baseline (T0) and after 12 ± 3 months (T1), including clinical evaluation, 12-item Kansas City Cardiomyopathy Questionnaire (KCCQ-12), symptom-limited bicycle exercise testing, and comprehensive echocardiography. The primary endpoint was change in quality of life (QoL). Secondary endpoints included exercise capacity, echocardiographic reverse remodelling, NYHA class, loop diuretic dose, and device-detected arrhythmias. Dose–response and multidimensional response patterns were explored. Results: KCCQ-12 increased from 52.96 ± 16.33 to 75.55 ± 18.12 (Δ +22.59 ± 13.22, p < 0.001), with 89.5% achieving a clinically meaningful improvement. Exercise duration and peak workload improved significantly. LVEF increased from 35.08 ± 6.96% to 43.18 ± 8.42% (Δ +8.11%, p < 0.001), with reductions in left ventricular and atrial volumes. Loop diuretic dose decreased (median −10 mg/day furosemide equivalent, p < 0.001), and 26.3% discontinued diuretics. A lower prevalence of device-detected arrhythmias was observed at follow-up, from 34.2% to 6.6% (p < 0.001). Higher ARNI doses were associated with greater likelihood of clinical, functional, and structural response. Longer CRT duration reduced the probability of structural remodelling but not symptomatic or functional benefit. Conclusions: In patients with long-standing CRT, delayed ARNI initiation was associated with improvements in QoL, exercise capacity, cardiac remodelling, congestion status, and electrical stability. These findings suggest that CRT is not a therapeutic ceiling and that late ARNI initiation remains a valuable component of comprehensive GDMT. Full article

The maintenance of endoplasmic reticulum (ER) Ca²⁺ homeostasis is intrinsically linked to the fidelity of protein folding, forming a functional tether that, when disrupted, triggers the Unfolded Protein Response (UPR). This bidirectional axis serves as a critical rheostat for cellular viability, yet its chronic dysregulation underpins the molecular etiology of numerous pathologies, including neurodegeneration, heart failure, and malignant transformation. This review provides a comprehensive interrogation of the Ca²⁺-ER Stress–UPR network, delineating how primary stress sensors—PERK, IRE1alpha, and ATF6—engage in complex feedback loops that either reinstate equilibrium or commit the cell to apoptosis. We specifically examine the PERK-CHOP-SERCA2b inhibitory circuit as a central driver of persistent Ca²⁺ depletion and discuss the role of Mitochondria-Associated Membranes (MAMs) in governing lethal Ca²⁺ transfer. Notably, we move beyond the classical paradigm of CHOP as a terminal apoptotic executioner, incorporating emerging evidence of its context-dependent adaptive functions. By synthesizing mechanistic insights across diverse disease models, this work highlights the transition from adaptive to maladaptive UPR as a universal pathological checkpoint. Ultimately, we evaluate the therapeutic potential of ‘axis-targeted’ interventions, such as SERCA activators and selective UPR modulators, aimed at resolving the underlying Ca²⁺ signaling defects in ER stress-related disorders. Full article

Artificial intelligence (AI) is rapidly reshaping adult cardiac surgery, enabling more accurate diagnostics, personalized risk assessment, advanced surgical planning, and proactive postoperative care. Preoperatively, deep-learning interpretation of ECGs, automated CT/MRI segmentation, and video-based echocardiography improve early disease detection and refine risk stratification beyond conventional tools such as EuroSCORE II and the STS calculator. AI-driven 3D reconstruction, virtual simulation, and augmented-reality platforms enhance planning for structural heart and aortic procedures by optimizing device selection and anticipating complications. Intraoperatively, AI augments robotic precision, stabilizes instrument motion, identifies anatomy through computer vision, and predicts hemodynamic instability via real-time waveform analytics. Integration of the Hypotension Prediction Index into perioperative pathways has already demonstrated reductions in ventilation duration and improved hemodynamic control. Postoperatively, machine-learning early-warning systems and physiologic waveform models predict acute kidney injury, low-cardiac-output syndrome, respiratory failure, and sepsis hours before clinical deterioration, while emerging closed-loop control and remote monitoring tools extend individualized management into the recovery phase. Despite these advances, current evidence is limited by retrospective study designs, heterogeneous datasets, variable transparency, and regulatory and workflow barriers. Nonetheless, rapid progress in multimodal foundation models, digital twins, hybrid OR ecosystems, and semi-autonomous robotics signals a transition toward increasingly precise, predictive, and personalized cardiac surgical care. With rigorous validation and thoughtful implementation, AI has the potential to substantially improve safety, decision-making, and outcomes across the entire cardiac surgical continuum. Full article

In today’s volatile digital environments, conventional data governance practices fail to adequately address the dynamic, context-sensitive, and risk-hazardous nature of data use. This paper introduces DRADG (Dynamic Risk-Adaptive Data Governance), a new paradigm that unites risk-aware decision-making with adaptive data governance mechanisms to enhance resilience, compliance, and trust in complex data environments. Drawing on the convergence of existing data governance models, best practice risk management (DAMA-DMBOK, NIST, and ISO 31000), and real-world enterprise experience, this framework provides a modular, expandable approach to dynamically aligning governance strategy with evolving contextual factors and threats in data management. The contribution is in the form of a multi-layered paradigm combining static policy with dynamic risk indicator through application of data sensitivity categorization, contextual risk scoring, and use of feedback loops to continuously adapt. The technical contribution is in the governance-risk matrix formulated, mapping data lifecycle stages (acquisition, storage, use, sharing, and archival) to corresponding risk mitigation mechanisms. This is embedded through a semi-automated rules-based engine capable of modifying governance controls based on predetermined thresholds and evolving data contexts. Validation was obtained through simulation-based training in cross-border data sharing, regulatory adherence, and cloud-based data management. Findings indicate that DRADG enhances governance responsiveness, reduces exposure to compliance risks, and provides a basis for sustainable data accountability. The research concludes by providing guidelines for implementation and avenues for future research in AI-driven governance automation and policy learning. DRADG sets a precedent for imbuing intelligence and responsiveness at the heart of data governance operations of modern-day digital enterprises. Full article

Aging involves progressive changes in sensory perception, appetite regulation, and metabolic flexibility, which together affect dietary intake, nutrient adequacy, and health-related outcomes. Meanwhile, current wearable technologies allow continuous, minimally invasive monitoring of physiological and behavioral markers relevant to metabolic health, such as physical activity, sleep, heart rate variability, glycemic patterns, and so forth. However, digital nutrition approaches have largely focused on physiological signals while underutilizing the sensory dimensions of eating—taste, smell, texture, and hedonic response—that strongly drive dietary intake and adherence. This narrative review synthesizes evidence on the following: (1) age-related sensory changes and their nutritional consequences, (2) metabolic adaptation and markers of resilience in older adults, and (3) current and emerging wearable technologies applicable to nutritional personalization. Following this, we propose an integrative framework linking subjective (implicit) sensory perception and objective (explicit) wearable-derived physiological responses into adaptive feedback loops to support personalized dietary strategies for healthy aging. In this light, we discuss practical applications, technological and methodological challenges, ethical considerations, and research priorities to validate and implement sensory–physiological integrated models. Merging together sensory science and wearable monitoring has the potential to enhance adherence, preserve nutritional status, and bolster metabolic resilience in aging populations, moving nutrition from one-size-fits-all prescriptions toward dynamic, person-centered, sensory-aware interventions. Full article

Tissue engineering is entering a new era, one defined not by passive scaffolds but by smart, adaptive biomaterials that can sense, think, and respond to their surroundings. These next-generation materials go beyond simply providing structure; they interact with cells and tissues in real time. Recent advances in mechanically responsive hydrogels and dynamic crosslinking have demonstrated how materials can adjust their stiffness, repair themselves, and transmit mechanical cues that directly influence cell behavior and tissue growth. Meanwhile, in vivo studies are demonstrating how engineered materials can harness the body’s own mechanical forces to activate natural repair programs without relying on growth factors or additional ligands, paving the way for minimally invasive, force-based therapies. The emergence of electroactive and conductive biomaterials has further expanded these capabilities, enabling two-way electrical communication with excitable tissues such as the heart and nerves, supporting more coordinated and mature tissue growth. Meanwhile, programmable bioinks and advanced bioprinting technologies now allow for precise spatial patterning of multiple materials and living cells. These printed constructs can adapt and regenerate after implantation, combining architectural stability with flexibility to respond to biological changes. This review brings together these cross-cutting advances, dynamic chemical design, mechanobiology-guided engineering, bioelectronic integration, and precision bio-fabrication to provide a comprehensive view of the path forward in this field. We discuss key challenges, including scalability, safety compliance, and real-time sensing validation, alongside emerging opportunities such as in situ stimulation, personalized electromechanical sites, and closed loop “living” implants. Taken together, these adaptive biomaterials represent a transformative step toward information-rich, self-aware scaffolds capable of guiding regeneration in patient-specific pathways, blurring the boundary between living tissue and engineered material. Full article