Vital pulp therapy (VPT) aims to preserve pulp vitality and stimulate regeneration of the dentin-pulp complex. Dental pulp stem cells (DPSCs) are clonogenic mesenchymal stem cells with high self-renewal and multipotent differentiation capacity. Bioactive cements such as mineral trioxide aggregate (MTA) and calcium-enriched mixture (CEM) are widely used as pulp-capping agents due to their biocompatibility. Platelet-rich fibrin (PRF), an autologous fibrin matrix rich in cytokines and growth factors, has been used to support tissue healing and regeneration.

Mast cells (MCs) play important roles in allergic reactions and tissue homeostasis; however, their functions in esophageal squamous cell carcinoma (ESCC) remain controversial. Understanding the heterogeneity and functional states of MCs in ESCC is essential for elucidating their roles in tumor progression and immune regulation.

Osteopetrosis is a rare genetic skeletal disorder caused by defective osteoclast-mediated bone resorption, leading to increased bone density and complications including hypocalcemia, pancytopenia, cranial nerve compression, and, more rarely, hydrocephalus. We report a rare case of intermediate osteopetrosis presenting with neonatal hypocalcemia and progressive macrocephaly. Brain magnetic resonance imaging confirmed obstructive hydrocephalus, which was treated with ventriculoperitoneal shunting. Clinical and radiological findings supported the diagnosis of osteopetrosis, although targeted genetic testing and whole exome sequencing did not identify a causative variant. The patient was treated with calcium gluconate and vitamin D supplementation, followed by hematopoietic stem cell transplantation from an HLA-matched unrelated donor using peripheral blood stem cells. This case highlights the importance of early recognition and timely hematopoietic stem cell transplantation to promote successful engraftment and improve long-term outcomes, even in the absence of molecular confirmation.

Following the publication of the above article and an Expression of Concern statement that was issued in light of concerns raised by an interested reader (doi: 10.3892/or.2025.9006) regarding the possible presentation of the same mouse twice in Fig. 7A, which showed how Bmi1 silencing suppresses the tumorigenicity of SP T24 cells in vivo, the authors have now responded to the enquiry posed by the Editorial Office. After consulting their original data, the authors have realized that the images of the first and third mouse in Fig. 7A were inadvertently mistakenly used during the manuscript preparation and figure editing stage. The authors were also asked to offer an explanation for the apparent discrepancy in the tumor sizes, given that the sizes of the tumors in situ appeared to be significantly larger than the measured sizes of the associated excised tumors. The authors acknowledged this concern, and attributed it to visual distortion from skin/fur, together with non‑standard approximate size recording practices at the time, while also admitting that detailed original measurement data were no longer available. The revised version of Fig. 7, now showing the correct mice in Fig. 7A, is shown on the next page. Note that the errors made in assembling this figure did not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [Oncology Reports 31: 727‑736, 2014; DOI: 10.3892/or.2013.2919].

Metabolic reprogramming is closely associated with the development and progression of cancer and is considered an emerging hallmark of cancer. To meet the bioenergetic and biosynthetic demands, tumor cells tend to initiate the metabolic reprogramming process, creating a tumor microenvironment that is adaptable for cancer cell growth and further promote oncogenic signaling, cell proliferation and metastasis. As a final byproduct of purine metabolism, the uric acid (UA) concentration rises in the quickly growing tumor microenvironment. However, whether elevated UA affects the development and prognosis of patients with tumors has not been demonstrated. In the present study, Cell Counting Kit‑8 and scratch healing test were used to investigate the effects of UA on the proliferation and migration of breast cancer cells. The effects of UA on nucleotide de novo synthesis genes in breast cells were validated using quantitative PCR (qPCR) and western blotting (WB). The activation of stemness in breast cancer cells by UA was validated using colony formation assays, ELISA, qPCR and WB. Finally, clinical data and The Cancer Genome Atlas database were analyzed to examine the expression of de novo nucleotide synthesis genes in cancerous and adjacent tissues, as well as in different types of breast cancer tissues. The present study investigated the potential effect of UA on the function of breast cancer; it also determined how UA affected the genes involved in nucleotide de novo synthesis, as well as how it contributes to tumor stemness. It was discovered that UA could enhance tumor stemness in breast cancer cells through the upregulation of guanosine 5'‑monophosphate synthase (GMPS). It was notable that GMPS expression in patients with breast cancer may be strongly associated with the course of the disease and the prognosis of patients. In conclusion, the present study demonstrated that elevated UA upregulates GMPS and stimulates the migration and proliferation of breast cancer cells through the cyclic guanosine monophosphate/protein kinase G/mitogen‑activated protein kinase pathway axis.

Hematopoietic stem and progenitor cells (HSPCs) sustain lifelong blood production, yet the molecular mechanisms underlying their functional decline with age remain incompletely understood. Understanding how aging alters the transcriptomic landscape of HSPCs is critical to uncovering the origins of immune system aging. We performed a comprehensive single-cell RNA sequencing analysis integrating over 300,000 bone marrow-derived HSPCs from 50 healthy individuals spanning 19 to 84 years of age. Aging was associated with immune lineage skewing, marked by increased myeloid and decreased lymphoid output in both bone marrow and peripheral blood. Subtle increases in HSCs, MEPs, and myeloid progenitors alongside reductions in lymphoid progenitors were already evident in aged bone marrow, suggesting that lineage bias is encoded at the progenitor level. Age-associated transcriptional changes included extensive upregulation of ribosomal genes encoding small (RPS11, RPS12, RPS23) and large (RPL9, RPL19, RPL24) cytoplasmic ribosomal subunit proteins, as well as pro-inflammatory mediators (IL1B, IL18, TGFB1, S100A8). Enrichment analysis identified mitochondrial function, ribosome biogenesis, chromatin remodeling, and inflammatory signaling as key ontologies disrupted during HSPC aging. Our study identifies molecular signatures of systemic aging rooted in bone marrow HSPCs and suggests that dysregulated ribosomal protein gene expression is an under-appreciated hallmark of hematopoietic stem cell aging.

Despite currently available treatment options for moderate-to-severe atopic dermatitis (AD), some patients fail to achieve adequate disease control. Emerging evidence suggests that mesenchymal stem cells (MSCs) may represent a promising therapeutic option. This systematic review and meta-analysis included four randomized controlled trials (RCTs) and one non-randomized clinical trial. Eligible studies evaluated patients with moderate-to-severe AD treated with MSCs derived from human umbilical cord blood, autologous adipose tissue, and allogeneic bone marrow. PubMed, Embase, and Cochrane were searched from inception to December 2025. Primary outcomes included the proportion of patients achieving ≥50% and ≥75% improvement from baseline in the Eczema Area and Severity Index (EASI) and safety outcomes. The meta-analysis included 236 participants. The pooled EASI-50 response rate at week 12 was 46.76% (95% confidence interval [CI]: 32.36% to 61.72%). EASI-75 response rates were 17.41% (95% CI: 5.56% to 43.03%) at week 12 and 23.97% (95% CI: 16.48% to 33.50%) at week 16. The pooled incidence of treatment-emergent adverse events was 26.86% (95% CI: 19.56% to 35.68%), with infections and infestations 7.97% (95% CI: 4.11% to 14.88%) and gastrointestinal disorders 3.52% (95% CI: 1.33% to 9.01%) being the most frequently reported. MSC-based therapy shows early promise as a potential treatment for moderate-to-severe AD, offering a possible alternative to traditional therapies. However, the current evidence is largely based on small clinical trials, underscoring the necessity for large-scale RCTs to establish the efficacy and safety of MSC-based therapy in broader patient populations.

Age-related metabolic dysregulation, chronic inflammation, and impaired vascularization severely compromise critical-sized bone healing. Building upon G-PLA nanocomposites previously established for bioelectronic encapsulation, we herein investigate their potential as a bio-instructive interface for guided bone regeneration. Fabricated via in situ graphite exfoliation, G-PLA provides enhanced hydrophilicity, mechanical robustness, and bioactivity while preserving excellent 3D-printability. In rat cranial defects, G-PLA significantly accelerated regeneration, as demonstrated by micro-CT, histological, and immunohistochemical analyses. Comparative evaluations in young and aged animals revealed that G-PLA effectively mitigates age-dependent declines in reparative capacity. Proteomic profiling indicated that G-PLA orchestrates a pro-regenerative microenvironment by inducing glycolytic reprogramming to meet the elevated energy demands of regeneration. In aged defects, G-PLA upregulated glycolytic enzymes (e.g., ALDOA and HK2), enhanced angiogenesis (CD31/CD34), and suppressed inflammation- and senescence-associated markers (e.g., P21 and SIRT2). In vitro studies validated that G-PLA augments glycolytic flux in endothelial cells, enhances osteogenic differentiation of mesenchymal stem cells, and promotes macrophage polarization toward an anti-inflammatory M2 phenotype. Therefore, G-PLA nanocomposites transcend passive structural support to act as a bio-instructive interface that revitalizes the aging-associated vascular-bone coupling, offering a versatile framework for next-generation multifunctional implantable hybrid systems.

Autologous cell-based approaches for bone repair using mesenchymal stromal cells (MSCs) in older patients are limited in part by cellular senescence, resulting in impaired MSC self-renewal and differentiation. Currently, the field lacks a standardized method to induce senescence in human MSCs and characterize them for experimental use, as well as effective strategies to mitigate the harmful effects of the senescence-associated secretory phenotype (SASP). We previously demonstrated that MSC-secreted decellularized extracellular matrix (dECM) enhances the osteogenic potential and survival of MSCs. We hypothesized that senescent MSCs would exhibit improved osteogenic potential and reduced SASP activity when maintained on dECM. We first demonstrated that a senescent phenotype can be reliably induced in human MSCs through ionizing irradiation coupled with a 21-day preconditioning phase in culture, evidenced by increased beta-galactosidase staining and enlarged cell area. We then observed that senescent MSCs on dECM exhibit improved osteogenic potential and reduced SASP compared to cells on tissue culture plastic, evidenced by quantifying markers of osteogenic differentiation and ELISAs for known inflammatory cytokines. These data support the promise of dECM as an instructive biomaterial to enhance the regenerative potential of MSCs from older patients for autologous bone repair.

Enamel, the outermost mineralized tissue of the tooth, is produced by specialized dental epithelial cells called ameloblasts. Unlike human enamel, which lacks regenerative capacity, the mouse incisor grows throughout life, driven by adult stem cells residing in the labial cervical loop (LaCl). To maintain tissue homeostasis, dental epithelial stem cells produce transit-amplifying cells (TACs) that commit to preameloblasts (PABs), migrate distally, and differentiate into enamel-forming ameloblasts. The full dental epithelial differentiation trajectory coexists within a single mouse incisor, making it an accessible model for studying adult tissue repair and regeneration. We have shown that the genome organizer SATB1 is enriched in PABs and is required for their differentiation into ameloblasts. Here, we investigated the injury response of PABs following mouse incisor tip trimming. Injured wild-type (wt) incisors exhibited an expanded PAB zone with intensive proliferation, reduced SATB1 in the ameloblast lineage, associated with a spatial delay in the deposition of the dentin/enamel matrix compared to uninjured controls. Trimming of Satb1 cKO mouse incisor failed to elicit this response, highlighting SATB1's role in PAB's response to injury. Compared with wt controls, injured wt incisors and both Satb1 cKO groups showed increased Ki67 immunoreactivity in LaCl mesenchymal and epithelial compartments, along with reduced Col1a1 expression in PAB microenvironment. In vitro, SATB1-transduced ameloblast lineage cells (ALCs) cultured on increasing concentrations of type I collagen exhibited reduced Ki67 but elevated Amelx/Ambn expression. There findings indicate that SATB1 is required for epithelial TACs to exit the cell cycle and transition toward PABs. Incisor tip injury delays PAB differentiation by stimulating LaCL mesenchymal proliferation and altering ECM remodeling within the PAB niche.

The developmental origins of health and disease (DOHaD) theory proposes that environmental exposure during critical periods of fetal and early postnatal development induces long-lasting biological changes that shape health trajectories across the lifespan. Hypertension and renal injury are adult-onset conditions associated with developmental programming that may increase the risk of non-communicable diseases later in life. Traditionally, reduced nephron endowment and subsequent glomerular hyperfiltration have been considered the principal mechanisms linking adverse fetal environments to subsequent hypertension and kidney disease. However, this paradigm does not fully explain the delayed onset or heterogeneity of these conditions. Accumulating evidence indicates that epigenetic regulation is a key mechanism by which early-life adversity is recorded. Renal stem and progenitor cells have emerged as cellular substrates for developmental programming, retaining information acquired during organogenesis, and influencing renal and vascular homeostasis later in life. Experimental studies have suggested that fetal malnutrition induces persistent epigenetic alterations in these cells, leading to altered differentiation, impaired repair capacity, and dysregulation of the intrarenal renin-angiotensin system, thereby increasing susceptibility to hypertension and renal injury in adulthood. Additionally, metabolic programming may interact with epigenetic regulation through sustained alterations in mitochondrial function and key metabolites. This mini-review summarizes the current evidence linking developmental programming to hypertension and renal injury, focusing on epigenetic regulation in renal stem and progenitor cells and metabolic alterations observed at the renal tissue level. We also discuss the reversibility, clinical implications for early life surveillance, and future directions for life-course strategies to prevent hypertension and renal injury. Graphical abstract. Developmental programming of hypertension and renal injury: epigenetic and metabolic memory. Adverse early-life environments, including fetal malnutrition, fetal growth restriction, ischemia, and prematurity, may program epigenetic memory in renal stem and progenitor cells and metabolic alterations in renal tissue. Epigenetic-metabolic interactions contribute to persistent abnormalities in renal mesenchymal stem cell (MSC) differentiation, intrarenal renin-angiotensin system (RAS) activation, injury-induced activation of label-retaining cells (LRCs), and endothelial progenitor cell (EPC)-mediated vascular repair. Postnatal nutrition, high salt intake, obesity, kidney injury, and ageing may amplify this vulnerability, promoting adult hypertension and renal injury and increasing long-term susceptibility to CKD. Maternal nutrition and supplementation, early surveillance, and lifestyle intervention represent potentially modifiable windows across the life course.

Cervical cancer remains one of the most prevalent gynecological malignancies worldwide, with high mortality rates particularly in developing countries, necessitating the development of effective and targeted therapeutic strategies. In this study, a folic acid (FA)-loaded amino-functionalized MCM-41 mesoporous silica nanocarrier was developed as a controlled delivery platform for cervical cancer applications. Pure MCM-41 was synthesized via a precipitation method and subsequently functionalized with aminopropyl groups through post-synthesis grafting, followed by FA-loading. Structural, textural and morphological analyses confirmed successful functionalization while maintaining the ordered mesoporous framework. In vitro drug release studies demonstrated pH-responsive behavior, with enhanced folic acid release under physiological conditions (pH 7.4) compared to acidic conditions (pH 1.5), supporting its suitability for controlled delivery applications. Cytotoxicity evaluation using HeLa cervical cancer cells and WI38 normal fibroblasts revealed selective anticancer activity of FA-functionalized systems with minimal toxicity toward normal cells. Among all formulations, the DMSO-based FA-loaded MCM-41 exhibited the highest cytotoxic and apoptotic effects, comparable to Doxorubicin. Mechanistic studies indicated that treatment induced oxidative stress through increased nitric oxide and malondialdehyde levels, accompanied by depletion of antioxidant enzymes (SOD and GSH). Additionally, apoptosis induction was confirmed by an increased Bax/Bcl-2 ratio and activation of the intrinsic mitochondrial pathway, along with suppression of PI3K/AKT survival signaling, along with downregulation of p-AKT. In conclusion, the developed FA-loaded amino-functionalized MCM-41 nanocarrier demonstrates efficient tumor targeting, controlled drug release, and potent apoptosis-mediated anticancer activity, highlighting its potential as a promising platform for cervical cancer therapy.

Perturbation of macropinocytosis triggers methuosis, a non-apoptotic cell death characterized by cytoplasmic vacuolization. However, the regulatory mechanisms of methuosis remain poorly defined. Lipid metabolism dysregulation is implicated in various cell death pathways, while its role in methuosis has remained elusive. Herein, LXX-8250, an isopropanolamine derivative of β-elemene, induced a vacuolization-associated cell death in breast and liver cancer cell lines. This process was accompanied by massive macropinocytosis, thereby confirming the occurrence of methuosis. Mechanistically, hypoxia-inducible lipid droplet-associated protein (HILPDA), a key regulator that promotes intracellular triacylglycerol (TAG) accumulation, was identified as the direct target of LXX-8250. By suppressing HILPDA, LXX-8250 inhibited diacylglycerol O-acyltransferase 1 (DGAT1) and activated adipose triglyceride lipase (ATGL). Consequently, lipid droplets and cellular TAG levels were reduced, while the subsequent increased diacylglycerol (DAG) stimulated macropinosome formation, leading to methuosis in these cells. In this study, we discover a novel methuosis agonist LXX-8250, and elucidate the critical role of HILPDA repression-dysregulated lipid metabolism in methuosis. Our study highlighted the potential of targeting this pathway as a therapeutic strategy to trigger cancer cell death.

Objective: To establish an in vitro fibrotic endometrial organoid model and investigate the early intervention effects of placenta-derived mesenchymal stem cell extracellular vesicles (Pd-MSC-EV) on fibrotic injury in endometrial organoids. Methods: Cell clusters were isolated from the endometrial tissues of healthy female mice and used to establish a three-dimensional endometrial organoid culture system. The structure and cellular composition of the organoids were characterized by histological staining and immunofluorescence staining. To construct an in vitro fibrosis model, the organoids were treated with different concentrations of transforming growth factor-β1 (TGF-β1), and model establishment was evaluated based on organoid morphological changes and the mRNA expression of fibrosis-related genes, including collagen type Ⅰ alpha 1 chain (COL1A1), α-smooth muscle actin (α-SMA), and fibronectin (FN). Pd-MSC-EVs were isolated and characterized by transmission electron microscopy, nanoparticle tracking analysis, and western blotting. The effects of Pd-MSC-EVs on TGF-β1-induced fibrotic changes in endometrial organoids were then assessed by morphological observation, real-time quantitative PCR (RT-qPCR) analysis of COL1A1, α-SMA, and FN mRNA expression, and immunofluorescence detection of COL1A1 and α-SMA protein expression. All experiments were repeated three times. Results: Mouse endometrial organoids with lumen-like structures were successfully established and expressed the epithelial markers E-cadherin and CK8 as well as the stromal marker Vimentin. Compared with the control group, TGF-β1 treatment disrupted organoid architecture and increased the mRNA expression levels of fibrosis-related genes, including COL1A1, α-SMA and FN, in a dose-dependent manner (all P<0.001). The isolated Pd-MSC-EV showed typical cup-shaped or disk-like vesicular morphology, with an average particle size of (163.8±50.0) nm, and expressed the exosomal markers CD63, CD81 and TSG101. Compared with the TGF-β1 group, co-treatment with Pd-MSC-EV alleviated organoid structural damage and reduced the mRNA expression levels of COL1A1, α-SMA and FN (all P<0.001). Immunofluorescence showed that COL1A1 protein expression was lower in the Pd-MSC-EV group than in the TGF-β1 group (P<0.005), while α-SMA protein expression showed a decreasing trend. Conclusion: Pd-MSC-EV attenuate TGF-β1-induced fibrotic changes in endometrial organoids in vitro and reduce organoid structural injury, providing experimental evidence for mechanistic studies and potential intervention strategies for endometrial fibrosis-related diseases such as intrauterine adhesions.

Ferroptosis has emerged as an important regulator of skeletal homeostasis, yet its role in osteoporosis (OP) remains incompletely understood. Accumulating evidence indicates that ferroptosis is not a uniform cell death program within bone, but rather a cell type-specific fate governed by distinct iron-handling capacities, redox buffering systems, and microenvironmental cues. This heterogeneity provides a new lens through which the complex pathogenesis of OP can be reinterpreted. In this review, we integrate recent advances to delineate ferroptosis-regulatory networks across major bone-resident cell populations, including osteoblasts, osteoclasts, osteocytes, and bone marrow mesenchymal stem cells (BMSCs). We highlight how ferroptosis suppresses osteogenic function in osteoblasts, amplifies differentiation and inflammatory signaling in osteoclasts, acts as an early vulnerability node in osteocytes, and reshapes lineage commitment in BMSCs. Importantly, ferroptosis in these cells is dynamically modulated by intercellular communication and niche-derived metabolic and mechanical signals. Building on this cell type-resolved framework, we propose that OP represents a disorder of multicellular ferroptotic dysregulation within the bone microenvironment rather than a simple imbalance of formation and resorption. Finally, we discuss translational implications, emphasizing ferroptosis-informed therapeutic strategies, including redox reprogramming, iron flux modulation, extracellular vesicle-based approaches, and microenvironment-responsive biomaterials. This integrative perspective provides a conceptual foundation for precision interventions targeting skeletal fragility across aging and disease contexts.

This study aimed to evaluate the cytocompatibility and transcriptional bioactivity profile of a calcium silicate-based endodontic sealer containing magnesium, in comparison with two widely used bioactive sealers, on immortalized human periodontal ligament stem cells (iPDLCs).

Structural remodeling of the dentate gyrus is a hallmark of temporal lobe epilepsy (TLE), yet the underlying molecular mechanisms remain incompletely understood. Nuclear distribution element-like 1 (Ndel1), a cytoskeleton-associated protein involved in neuronal migration and dendritic development, has not been characterized in dentate gyrus remodeling during epileptogenesis. Here, we investigated region- and cell-type-specific alterations in Ndel1 expression in a pilocarpine-induced mouse model of TLE and examined the effects of adeno-associated virus (AAV)-mediated Ndel1 expression on structural remodeling. Immunofluorescence was used to define Ndel1 localization across neural stem cells, granule lineage cells, mature neurons, and astrocytes, and dendritic architecture was assessed using Golgi staining and Sholl analysis. Total hippocampal Ndel1 expression increased after status epilepticus, whereas Ndel1-positive cells decreased selectively in the subgranular zone but increased among granule lineage cells in the hilus. Ndel1 was preferentially expressed in BLBP-positive neural stem cells and mature neurons, but not in neuroblasts. Activated astrocytic processes exhibited increased spatial association with Ndel1-positive cells during early remodeling. Ndel1 overexpression was associated with partial normalization of neuronal marker distribution, increased dendritic spine density, and reduced dendritic branching complexity. These findings suggest that Ndel1 is associated with region- and lineage-specific structural remodeling in the dentate gyrus during epileptogenesis.

Prostate cancer (PCa) is a leading cause of male cancer mortality worldwide. Its treatment failure is predominantly driven by the transition to castration-resistant phenotype (CRPC). Zinc finger E-box binding homeobox 1 (ZEB1) is a master inducer of epithelial-mesenchymal transition and has emerged as a central orchestrator of malignant phenotype. This review clarifies the complex interplay between ZEB1 and the tumor microenvironment, epigenetic modifications, and non-coding RNAs (lncRNAs and miRNAs), highlighting how these interactions collectively drive the progression of PCa. Moreover, ZEB1 is critical in driving the transformation of cancer cells to cancer stem cells and promoting neuroendocrine differentiation. This review highlights ZEB1 to resistance against standard-of-care treatments (such as taxane-based chemotherapies and next-generation androgen receptor pathway inhibitors) by metabolic reprogramming and modulation of androgen receptor signaling. Finally, it explores strategies to disrupt the regulatory circuitry of ZEB1 to overcome multidrug resistance, with the specific aim of evaluating whether ZEB1 can serve as a viable clinical biomarker and therapeutic target for PCa treatment.

Elastic cartilage is essential for preserving the structural integrity and functional flexibility of tissues such as the auricle and epiglottis. However, its limited capacity for self-repair poses significant challenges in the treatment of injuries resulting from trauma, congenital defects, or disease. This study investigates the in vitro and in vivo regenerative potential of a bioink designed for auricular cartilage repair. The primary polymeric components of the bioink were κ-carrageenan and silk fibroin (κ-CA/SF), while the cellular component consisted of adipose-derived stem cells (ADMSCs) isolated from rabbits, which were subsequently seeded onto poly(butylene adipate-co-terephthalate) (PBAT) microcarriers. These components were successfully printed utilizing an extrusion-based bioprinter. In vitro analyses demonstrated that ADMSCs were effectively encapsulated within the bioink, maintaining their viability for a duration of 21 days. Quantitative RT-qPCR analyses confirmed the expression of COL2A1, the major structural protein of cartilage and a critical indicator of the chondrocyte phenotype; its expression was observed to be approximately 35-fold higher in the κ-CA/SF + PBAT group compared to the κ-CA/SF group (***p < 0.001). Additionally, the presence of collagen II and aggrecan within the constructs was confirmed through immunostaining. For in vivo experiments, a circular defect in auricular cartilage, encompassing the perichondrium on both sides, was created in New Zealand rabbits to facilitate the implantation of tissue scaffolds. Cartilage regeneration was evaluated through histological staining at 4 and 8 weeks post-implantation. In the κ-CA/SF + PBAT group, distinct microcircular structures were identified within the connective tissue, and at later time points, the defect area was predominantly populated with mature cartilage cells, indicating advanced tissue development.