This study reports, for the first time, lanthanum oxide (La₂O₃) nanoparticles (NPs) that simultaneously suppress osteosarcoma MG63 cell proliferation and promote normal Vero cell viability, a dual effect not previously documented for La₂O₃ or similar metal oxide NPs. Physico-chemical characterization revealed a unique needle-like morphology, cubic crystallinity, and dispersion stability in DMSO without acidic dispersants, properties that can influence cellular uptake, ROS modulation, and biocompatibility. Comprehensive characterization (fluorescence spectroscopy, particle size/zeta potential, Raman, XRD, TGA, ATR-FTIR, and TEM) confirmed structural stability and surface chemistry relevant to biological interactions.La₂O₃ NPs exhibited broad-spectrum antibacterial activity (Gram-positive Streptococcus pyogenes, Bacillus cereus; Gram-negative Escherichia coli, Pseudomonas aeruginosa) and strong enzymatic/non-enzymatic antioxidant capacity, supporting potential use in implant coatings and infection control. MTT assays demonstrated dose-dependent cytotoxicity in MG63 cells, with enhanced proliferation in Vero cells. In zebrafish embryos, developmental toxicity assays yielded an LC₅₀ of 2.6 mg/mL higher (less toxic) than values reported for Ag NPs (~0.3–1 mg/mL) with normal development at lower concentrations and dose-dependent malformations (e.g., impaired somite formation and skeletal deformities) at higher doses. Collectively, these findings position La₂O₃ NPs as a multifunctional platform for oncology and regenerative medicine, uniquely combining selective anticancer activity, normal cell support, antimicrobial and antioxidant functions, and a defined developmental safety margin.

Organ transplantation serves as a critical life-saving intervention. However, the persistent global shortage of donor organs continues to result in high mortality rates. This pressing clinical challenge has fueled the search for alternative therapeutic strategies. Among these strategies, three-dimensional (3D) bioprinting has emerged as a transformative technology capable of fabricating complex tissue constructs using bioinks composed of living cells and supportive biomaterials. Notably, recent advancements have highlighted the incorporation of decellularized extracellular matrix (dECM) as a bioactive component, significantly enhancing biocompatibility, structural integrity, cellular support, and the formation and maturation of vascular networks. In this review, we detail the pivotal role of the extracellular matrix (ECM) as a dynamic reservoir of biochemical signals and mechanical cues that regulate cellular behavior through mechanotransduction. These processes guide essential functions including gene expression, tissue development, and remodeling, thereby ensuring tissue-specific mechanical properties such as elasticity and tensile strength. We highlight how dECM-based bioinks can retain the native structural and molecular features of the ECM, making them ideal for replicating physiologically relevant microenvironments. Representative studies demonstrate the successful application of dECM bioinks in engineering complex in vitro 3D tissue models. Furthermore, we address current challenges in tissue engineering, including the standardization of bioink formulations, refinement of decellularization techniques, and enhancement of the mechanical and architectural properties of scaffolds. Finally, we explore emerging solutions—such as artificial intelligence (AI) -guided optimization, in situ bioprinting, and the development of patient-specific bioinks—as promising avenues to overcome current limitations and drive the clinical translation of 3D bioprinted tissues.

This book chapter on neurodegeneration research provides an explicit discussion on the present scenario, challenges, and future directions in the field. The chapter delves into critical insights into disease pathogenesis, therapeutic interventions, ethical considerations, and clinical trials, offering a holistic perspective on the complexities of neurodegenerative disorders. By exploring ethical frameworks, clinical translation, global health implications, and collaborative endeavors, the chapter underscores the importance of interdisciplinary approaches, patient-centered care, and innovative technologies in driving progress towards understanding, diagnosing, and treating neurodegeneration. As researchers, healthcare providers, policymakers, and stakeholders continue to navigate ethical dilemmas, translate scientific discoveries into clinical practice, and address global health disparities, the collective efforts in neurodegeneration research aim to improve outcomes, enhance patient care, and ultimately make a meaningful impact on individuals affected by these challenging conditions.

Parkinson’s disease (PD), a progressive neurodegenerative disorder, is increasingly recognized as a disorder of accelerated cellular aging, driven by telomere shortening, cellular senescence, mitochondrial dysfunction, and chronic neuroinflammation. Central to its pathophysiology is the accumulation of α-synuclein aggregates, which trigger astrocyte and microglial senescence, leading to the secretion of pro-inflammatory SASP factors and creating a toxic neural microenvironment. These processes are tightly interwoven with mitochondrial impairment and the generation of reactive oxygen species (ROS), which accelerate telomere attrition and perpetuate neuronal loss through a self-reinforcing feedback loop. Dysregulation of key molecular regulators such as telomerase reverse transcriptase (TERT), GBA mutations, and the SATB1-miR22 axis further exacerbate lysosomal dysfunction, senescence, and α-synuclein accumulation. TERT, though neuroprotective when upregulated, is often downregulated in PD, while GBA mutations impair autophagy and contribute to a senescence-like phenotype in dopaminergic neurons. The SATB1-miR22-GBA network links epigenetic regulation to lysosomal failure and cellular aging. These interconnected mechanisms illuminate a multifactorial model of PD pathogenesis where senescence and telomere instability serve as central hubs. Therapeutic strategies targeting telomerase activation, clearance of senescent cells via senolytics, and modulation of the GBA/SATB1-miR22 pathway represent promising avenues for mitigating neurodegeneration and improving clinical outcomes in aging-related neurodegenerative diseases such as PD.v