Nanographene Oxide Promotes Angiogenesis by Regulating Osteoclast Differentiation and Platelet-Derived Growth Factor Secretion.

An imbalanced system of angiogenesis-osteoblasts-osteoclasts is regarded as the main factor in bone remodeling dysfunction diseases or osseointegration loss. Osteoclast precursors are the key cells that accelerate bone-specific angiogenesis and maintain normal osteoblast and osteoclast function. Graphene oxide is an effective scaffold surface modification agent with broad application prospects in bone tissue engineering.

Nanomaterials-induced programmed cell death: Focus on mitochondria.

Nanomaterials are widely utilized in several domains, such as everyday life, societal manufacturing, and biomedical applications, which expand the potential for nanomaterials to penetrate biological barriers and interact with cells. Multiple studies have concentrated on the particular or improper utilization of nanomaterials, resulting in cellular death. The primary mode of cell death caused by nanotoxicity is programmable cell death, which includes apoptosis, ferroptosis, necroptosis, and pyroptosis.

Graphene-Based Material-Mediated Immunomodulation in Tissue Engineering and Regeneration: Mechanism and Significance.

Tissue engineering and regenerative medicine hold promise for improving or even restoring the function of damaged organs. Graphene-based materials (GBMs) have become a key player in biomaterials applied to tissue engineering and regenerative medicine. A series of cellular and molecular events, which affect the outcome of tissue regeneration, occur after GBMs are implanted into the body.

MDM2 upregulation induces mitophagy deficiency via Mic60 ubiquitination in fetal microglial inflammation and consequently neuronal DNA damage caused by exposure to ZnO-NPs during pregnancy.

During pregnancy, the human body is quite vulnerable to external stimuli. Zinc oxide nanoparticles (ZnO-NPs) are widely used in daily life, and they enter the human body via environmental or biomedical exposure, thus having potential risks. Although accumulating studies have demonstrated the toxic effects of ZnO-NPs, few studies have addressed the effect of prenatal ZnO-NP exposure on fetal brain tissue development.

Tongue-Brain-Transported ZnO Nanoparticles Induce Abnormal Taste Perception.

Nanoparticles (NPs) can be transported to the brain, especially through nerves, because of their small size and high biological activity. Previous studies confirmed that zinc oxide (ZnO) NPs can enter the brain through the tongue-brain pathway, but it is unclear whether they will further affect synaptic transmission and brain perception. In this study, it is found that tongue-brain-transported ZnO NPs can cause a decrease in taste sensitivity and taste aversion learning ability, indicating abnormal taste perception.

How Nanoparticles Open the Paracellular Route of Biological Barriers: Mechanisms, Applications, and Prospects.

Biological barriers are essential physiological protective systems and obstacles to drug delivery. Nanoparticles (NPs) can access the paracellular route of biological barriers, either causing adverse health impacts on humans or producing therapeutic opportunities. This Review introduces the structural and functional influences of NPs on the key components that govern the paracellular route, mainly tight junctions, adherens junctions, and cytoskeletons.

Nanomaterials alleviating redox stress in neurological diseases: mechanisms and applications.

Overproduced reactive oxygen and reactive nitrogen species (RONS) in the brain are involved in the pathogenesis of several neurological diseases, such as Alzheimer's disease, Parkinson's disease, traumatic brain injury, and stroke, as they attack neurons and glial cells, triggering cellular redox stress. Neutralizing RONS, and, thus, alleviating redox stress, can slow down or stop the progression of neurological diseases. Currently, an increasing number of studies are applying nanomaterials (NMs) with anti-redox activity and exploring the potential mechanisms involved in redox stress-related neurological diseases.

Improvement of synaptic plasticity by nanoparticles and the related mechanisms: Applications and prospects.

Synaptic plasticity is an important basis of learning and memory and participates in brain network remodelling after different types of brain injury (such as that caused by neurodegenerative diseases, cerebral ischaemic injury, posttraumatic stress disorder (PTSD), and psychiatric disorders). Therefore, improving synaptic plasticity is particularly important for the treatment of nervous system-related diseases. With the rapid development of nanotechnology, increasing evidence has shown that nanoparticles (NPs) can cross the blood-brain barrier (BBB) in different ways, directly or indirectly act on nerve cells, regulate synaptic plasticity, and ultimately improve nerve function.

Nano-graphene oxide depresses neurotransmission by blocking retrograde transport of mitochondria.

The application of graphene-family nanomaterials (GFNs) in neuromedicine has recently gained increased attention, but the associated exposure risk for synaptic function and the underlying mechanism remains obscure. The results of this study utilizing nanosized graphene oxide (nGO) suggest that they exert depressive effects on neurotransmission, mainly due to energy deficiency at synaptic contacts. Mitophagy is activated but fails to renew mitochondria and maintain mitochondrial-mediated energy metabolism because of blockage of autophagosome transport through the microtubule system from the axonal terminal to the soma.

Understanding the interactions between inorganic-based nanomaterials and biological membranes.

The interactions between inorganic-based nanomaterials (NMs) and biological membranes are among the most important phenomena for developing NM-based therapeutics and resolving nanotoxicology. Herein, we introduce the structural and functional effects of inorganic-based NMs on biological membranes, mainly the plasma membrane and the endomembrane system, with an emphasis on the interface, which involves highly complex networks between NMs and biomolecules (such as membrane proteins and lipids). Significant efforts have been devoted to categorizing and analyzing the interaction mechanisms in terms of the physicochemical characteristics and biological effects of NMs, which can directly or indirectly influence the effects of NMs on membranes.

Nanomaterials and hepatic disease: toxicokinetics, disease types, intrinsic mechanisms, liver susceptibility, and influencing factors.

The widespread use of nanomaterials (NMs) has raised concerns that exposure to them may introduce potential risks to the human body and environment. The liver is the main target organ for NMs. Hepatotoxic effects caused by NMs have been observed in recent studies but have not been linked to liver disease, and the intrinsic mechanisms are poorly elucidated.

Tantalum Particles Induced Cytotoxic and Inflammatory Effects in Human Monocytes.

The aim of this study is to evaluate the biological safety of tantalum (Ta) particles and to further explore the effects of Ta particles on human monocyte toxicity and inflammatory cytokine expression. Human monocyte leukemia (THP-1) cells were cultured with Ta and hydroxyapatite (HA) particles. Cell counting kit-8 method was used to evaluate the cytotoxicity of Ta and HA particles.

Effects of carbon-based nanomaterials on vascular endothelia under physiological and pathological conditions: interactions, mechanisms and potential therapeutic applications.

The endothelium participates in maintaining vascular hemostasis and is involved in multiple pathological processes. Although it is rarely the targeted tissue, the endothelium interacts intimately with applied therapeutic systems. Carbon nanomaterials (CBNs) with editable physiochemical characteristics and outstanding biosafety are believed to have great prospects in the biomedical field.

Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1.

Cartilage defects in temporomandibular disorders (TMD) lead to chronic pain and seldom heal. Synovium-derived mesenchymal stem cells (SMSCs) exhibit superior chondrogenesis and have become promising seed cells for cartilage tissue engineering. However, local inflammatory conditions that affect the repair of articular cartilage by SMSCs present a challenge, and the specific mechanism through which the function remains unclear.

Dual effects of JNK activation in blood-milk barrier damage induced by zinc oxide nanoparticles.

Zinc oxide nanoparticles (ZnO-NPs) have been extensively applied in our daily life. Humans are at high risk of being exposed to ZnO-NPs, which induce potentially adverse health effects. Although a growing number of studies have investigated the toxic effects of ZnO-NPs, the available data concerning ZnO-NP interactions with the blood-milk barrier (BMB) remain highly limited.

Oxidation of Reduced Graphene Oxide Cellular Redox Signaling Modulates Actin-Mediated Neurotransmission.

Neurotransmission is the basis of brain functions, and controllable neurotransmission tuning constitutes an attractive approach for interventions in a wide range of neurologic disorders and for synapse-based therapeutic treatments. Graphene-family nanomaterials (GFNs) offer promising advantages for biomedical applications, particularly in neurology. Our study suggests that reduced graphene oxide (rGO) serves as a neurotransmission modulator and reveals that the cellular oxidation of rGO plays a crucial role in this effect.

Interactions of nanomaterials with ion channels and related mechanisms.

The pharmacological potential of nanotechnology, especially in drug delivery and bioengineering, has developed rapidly in recent decades. Ion channels, which are easily targeted by external agents, such as nanomaterials (NMs) and synthetic drugs, due to their unique structures, have attracted increasing attention in the fields of nanotechnology and pharmacology for the treatment of ion channel-related diseases. NMs have significant effects on ion channels, and these effects are manifested in many ways, including changes in ion currents, kinetic characteristics and channel distribution.

Key Role of Microtubule and Its Acetylation in a Zinc Oxide Nanoparticle-Mediated Lysosome-Autophagy System.

Autophagy is a biological process that has attracted considerable attention as a target for novel therapeutics. Recently, nanomaterials (NMs) have been reported to modulate autophagy, which makes them potential agents for the treatment of autophagy-related diseases. In this study, zinc oxide nanoparticles (ZNPs) are utilized to evaluate NM-induced autophagy and debate the mechanisms involved.

Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the Ca-dependent NF-κB and MAPK pathways.

Background: The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known.

The toxicity of silica nanoparticles to the immune system.

Silicon-based materials and their oxides are widely used in drug delivery, dietary supplements, implants and dental fillers. Silica nanoparticles (SiNPs) interact with immunocompetent cells and induce immunotoxicity. However, the toxic effects of SiNPs on the immune system have been inadequately reviewed.

Nanoscaffolds in promoting regeneration of the peripheral nervous system.

The ability to surgically repair peripheral nerve injuries is urgently needed. However, traditional tissue engineering techniques, such as autologous nerve transplantation, have some limitations. Therefore, tissue engineered autologous nerve grafts have become a suitable choice for nerve repair.

Zinc oxide nanoparticles induce toxic responses in human neuroblastoma SHSY5Y cells in a size-dependent manner.

Due to the widespread applications of zinc oxide nanoparticles (ZnO NPs), the potential exposure of workers, consumers, and scientists to these particles has increased. This potential for exposure has attracted extensive attention in the science community. Many studies have examined the toxicological profile of ZnO NPs in the immune system, digestive system, however, information regarding the toxicity of ZnO NPs in the nervous system is scarce.