Wound repair preserves tissue integrity through four overlapping phases—hemostasis, inflammation, proliferation, and remodeling—coordinated by platelets, neutrophils, macrophages, fibroblasts, keratinocytes, endothelial cells, and stem/progenitor cells acting with growth factors, chemokines, extracellular matrix, and intracellular signaling. Disruption of these programs results in chronic non-healing wounds or fibrotic scarring. Recent work delineates microbial influences, epigenetic and transcriptomic regulation, and cellular heterogeneity resolved by single-cell and spatial omics. Concurrent advances in biomaterials, engineered scaffolds, stem cell-derived products, and genome-targeted approaches are enabling mechanism-based therapies. Persistent challenges include wound heterogeneity, systemic modifiers such as diabetes and aging, and safe, effective delivery of biologics. This review summarizes cellular and molecular mechanisms of cutaneous repair, outlines deviations that underlie pathological healing, and evaluates emerging concepts and translational strategies. Integrating classical models with contemporary insights supports the development of precision wound medicine and personalized interventions to improve outcomes and quality of life.

Decellularized extracellular matrix (dECM) scaffolds preserve native tissue structure and biochemical cues while minimizing immune responses, creating biomimetic templates that promote cell integration and tissue remodeling. This review examines the current state of dECM research, encompassing decellularization methods, scaffold quality evaluation assays, and tissue-specific applications across dermis, nerve, heart, lung, adipose, and placental ECMs. We analyze commercially available dECM products and ongoing clinical trials, while highlighting recent advances including 3D bioprinting and the integration of dECM with stem cells and growth factors. Despite these promising developments, several challenges continue to limit broader clinical translation: protocol standardization, residual immunogenicity, mechanical durability, and regulatory, manufacturing, and cost barriers. To address these limitations, we outline future directions focusing on patient-specific scaffolds, scalable bioprocessing, and integrated biofabrication strategies that will enable the development of safe and effective dECM-based therapies.

Tissue engineering and regenerative medicine are shifting from passive tissue replacement toward instructive platforms that regulate cellular behavior, immune responses, vascularization, and extracellular matrix remodeling. This review examines recent advances in natural, synthetic, composite, and stimuli-responsive biomaterials, biofabrication and 3D bioprinting, stem and progenitor cell therapies, extracellular vesicles and other cell-free products, immunomodulatory scaffolds, skin organoids and organ-on-a-chip systems, nanotechnology, and artificial intelligence-assisted design. Particular emphasis is placed on plastic, reconstructive, and aesthetic applications, including skin and wound repair, craniofacial bone and cartilage regeneration, peripheral nerve reconstruction, vascularization, and dental and periodontal repair. The review also considers biomodulators and skinboosters as emerging regenerative-aesthetic interventions that aim to improve dermal hydration, fibroblast activity, collagen remodeling, and skin quality rather than provide volume replacement alone. Importantly, these technologies differ substantially in translational maturity, ranging from in vitro and preclinical platforms to early clinical interventions, established clinical products, and commercially available treatments for which durable regenerative efficacy remains incompletely validated. Throughout this review, biological plausibility and preclinical efficacy are therefore distinguished from human clinical evidence, regulatory or established clinical use, and commercial availability. Progress will require standardized characterization, mechanism-linked potency assays, clinically relevant models, and outcome measures that capture functional integration, durability, safety, and aesthetic performance.

Wound healing remains a significant clinical challenge worldwide, and effective management strategies are essential for improving outcomes. This study evaluated SCderm Matrix, a novel acellular dermal matrix (ADM) patch developed using supercritical carbon dioxide (sCO₂) processing of human skin tissue. This innovative processing method preserves structural integrity while enhancing biocompatibility, resulting in a patch characterized by porous architecture, uniform thickness, excellent tensile strength, and optical transparency. In vivo wound healing experiments using full-thickness skin wounds in Sprague–Dawley rats demonstrated the patch’s superior performance. Treatment with the sCO₂ ADM patch accelerated wound closure, reduced inflammation, and enhanced granulation tissue formation compared to both untreated controls and two commercially available ADM products. Histological analysis revealed improved re-epithelialization and collagen deposition, while molecular and immunohistochemical assessments showed decreased reactive oxygen species (ROS) and pro-inflammatory cytokines. Simultaneously, the treatment upregulated key proliferation and remodeling markers including alpha smooth muscle actin (α-SMA), vimentin, and transforming growth factor beta 1 (TGF-β1). These findings demonstrate that the SCderm Matrix promotes wound healing through multiple mechanisms: modulating inflammatory responses, enhancing antioxidant defenses, and supporting tissue regeneration. The results suggest this biomaterial has significant potential as an effective and versatile solution for clinical wound care applications.

Objective: This study was to evaluate the effects of a composite extract of Prunus mume flower, Lonicera japonica flower (honeysuckle), Chrysanthemum indicum flower, and Phyllostachys bambusoides , which we named PLCP, on skin hydration, inflammation, itching, and oxidative stress in pediatric (NHEK) and adult (HaCaT) keratinocytes. Methods: LPS was used to simulate the external stimulation for pediatric (NHEK) and adult (HaCaT) keratinocytes. These keratinocytes were treated with different concentrations of PLCP, and the expression of inflammation, itching, and oxidative stress‐related proteins or mRNA was observed through rt‐PCR, ELISA, ROS, and SOD. Meanwhile, rt‐PCR was also used to determine the expression of Hyaluronic acid synthase (HAS) in keratinocytes under PLCP intervention for its moisturizing effects. Results: PLCP treatment (0.125%–0.500%) significantly suppressed LPS‐stimulated thymic stromal lymphopoietin (TSLP) secretion by up to 40.3% in pediatric cells and 29.9% in adult cells ( p < 0.05), and reduced endothelin‐1 (ET‐1) mRNA levels by up to 69.5% and 46.0%, respectively ( p < 0.05). Concurrently, PLCP dose‐dependently upregulated hyaluronic acid synthase isoforms (HAS‐1, HAS‐2, HAS‐3) mRNA expression by 174.8%–254.2% in pediatric keratinocytes and 143.5%–198.9% in adult cells ( p < 0.05), indicating enhanced hydration potential. Antioxidant assays demonstrated that PLCP at 0.250% decreased reactive oxygen species (ROS) by 55.3% in pediatric and 41.6% in adult cells, while boosting superoxide dismutase (SOD) activity ( p < 0.05). Conclusions: Across all endpoints, pediatric keratinocytes exhibited more pronounced responses, suggesting age‐dependent differences in sensitivity. These in vitro findings support PLCP's multifunctional role at anti‐inflammatory, anti‐pruritic, moisturizing, and antioxidant and highlight its promise as a safe, plant‐based alternative for managing pediatric skin disorders.

Atopic dermatitis (AD) is a chronic, relapsing inflammatory dermatosis characterized by pruritus, eczematous lesions, and a fluctuating course. It imposes substantial quality-of-life and economic burdens through sleep disturbance, pain, psychosocial distress, and frequent healthcare utilization. Recent global estimates suggest AD affects hundreds of millions worldwide, with meaningful prevalence in both children and adults. AD pathogenesis is multifactorial, reflecting the interaction of genetic predisposition, immune dysregulation dominated by type 2 inflammation, epidermal barrier impairment, neuroimmune itch pathways, and microbial dysbiosis. Clinical diagnosis remains primarily clinical, supported by classic criteria emphasizing pruritus, typical morphology, chronicity, and atopic history. Disease severity and treatment response are commonly quantified using validated measures such as EASI and SCORAD, enabling standardized monitoring and evidence-based escalation. Management has shifted from broad immunosuppression to a stepwise, endotype-aware approach integrating barrier repair, anti-inflammatory topical therapy, phototherapy, conventional systemic agents, and rapidly expanding targeted options. Recent guidelines and approvals highlight increasing roles for biologics and JAK pathway inhibition, alongside newer nonsteroidal topicals. This review summarizes current concepts and practical treatment integration, with emphasis on safety, monitoring, and future research directions.