(1) Background: Acute ischemic stroke (IS) is one of the main causes of human disability and death. Therefore, multifunctional nanosystems that effectively cross the blood–brain barrier (BBB) and efficiently eliminate reactive oxygen species (ROS) are urgently needed for comprehensive neuroprotective effects. (2) Methods: We designed a targeted transferrin (Tf)-based manganese dioxide nanozyme (MnO₂@Tf, MT) using a mild biomimetic mineralization method for rebalancing ROS levels. Furthermore, MT can be efficiently loaded with edaravone (Eda), a clinical neuroprotective agent, to obtain the Eda-MnO₂@Tf (EMT) nanozyme. (3) Results: The EMT nanozyme not only accumulates in a lesion area and crosses the BBB but also possesses satisfactory biocompatibility and biosafety based on the functional inheritance of Tf. Meanwhile, EMT has intrinsic hydroxyl radical-scavenging ability and superoxide-dismutase-like and catalase-like nanozyme abilities, allowing it to ameliorate ROS-mediated damage and decrease inflammatory factor levels in vivo. Moreover, the released Mn²⁺ ions in the weak acid environment of the lesion area can be used for magnetic resonance imaging (MRI) to monitor the treatment process. (4) Conclusions: Our study not only paves a way to engineer alternative targeted ROS scavengers for intensive reperfusion-induced injury in ischemic stroke but also provides new insights into the construction of bioinspired Mn-based nanozymes.

In the past few decades, brain diseases have taken a heavy toll on human health and social systems. Magnetic resonance imaging (MRI), photoacoustic imaging (PA), computed tomography (CT), and other imaging modes play important roles in disease prevention and treatment. However, the disadvantages of traditional imaging mode, such as long imaging time and large noise, limit the effective diagnosis of diseases, and reduce the precision treatment of diseases. The ever-growing applications of inorganic nanomaterials in biomedicine provide an exciting way to develop novel imaging systems. Moreover, these nanomaterials with special physicochemical characteristics can be modified by surface modification or combined with functional materials to improve targeting in different diseases of the brain to achieve accurate imaging of disease regions. This article reviews the potential applications of different types of inorganic nanomaterials in vivo imaging and in vitro detection of different brain disease models in recent years. In addition, the future trends, opportunities, and disadvantages of inorganic nanomaterials in the application of brain diseases are also discussed. Additionally, recommendations for improving the sensitivity and accuracy of inorganic nanomaterials in screening/diagnosis of brain diseases.

Ceria nanoparticles (CeO₂NPs) exhibit great potential in cardiovascular disease and nonalcoholic fatty liver disease due to its excellent antioxidant capacity. However, the profitable effect of CeO₂NPs on many diseases is almost all attributed to the regulation of ROS. Apart from the general antioxidant function, there seems to be no more distinct mechanism to reflect its unique multi-disease improvement effect. Here, we for the first time reveal a new discovery of CeO₂NPs in mimicking nitric oxide synthase (NOS) by catalyzing L-arginine (L-Arg) to produce nitric oxide (NO) or the derivatives. NOS-like activity of CeO₂NPs is original and associated with multiple factors like substrate concentration, pH, temperature and time, etc. where oxygen vacancy ratio plays a more critical role. Meanwhile, NOS-like activity of CeO₂NPs successfully elevates NO secretion in endothelial cells and macrophages without expanding eNOS/iNOS expression. Importantly, NOS-like activity of CeO₂NPs and the responsive endogenous NO promote the re-distribution of blood lipids and stabilize eNOS expression but suppress iNOS, thus collectively alleviate the accumulation of vascular plaque. Altogether, we provide a new angle of view to survey the outstanding potential of CeO₂NPs, apart from the inevitable antioxidant capacity, the covert but possible and more critical NOS-like enzymatic activity is more noteworthy.

Ischemia–reperfusion (I/R) injury in skin flap transplantation causes acute oxidative damage and inflammation, leading to high failure rates and tissue necrosis. Herein, we present a core–shell Pd@CeO₂ nanozymes that addresses this challenge via a unique electron-injection mechanism across the Pd–CeO₂ interface, conferring unprecedented antioxidant and anti-inflammatory potency. Constructed by confining Pd clusters within a ceria matrix, this nanozyme combines catalase- and superoxide dismutase–like catalytic activities for robust reactive oxygen species (ROS) scavenging. In vitro, Pd@CeO₂ rapidly neutralizes ROS, preventing oxidative cell death by reducing apoptosis and dampening inflammatory signaling, while restoring angiogenic potential. In a rat skin flap I/R model, Pd@CeO₂ significantly improves flap survival and microvascular regeneration while concurrently reducing tissue necrosis, apoptosis, and inflammation, with no observable toxicity. By simultaneously alleviating oxidative stress, cell death, inflammation, and vascular dysfunction, this nanozyme offers a comprehensive therapeutic strategy against I/R injury. This work introduces a new paradigm for nanozyme-based cytoprotection in transplantation, with potential applicability to other ischemic injuries.

Wearable electronics can achieve high‐fidelity monitoring of pulse waveforms on the body surface enabling early diagnosis of cardiovascular diseases (CVDs). Textile‐based wearable devices offer advantages in terms of high permeability and comfort. However, knitted strain sensors struggle to capture small‐range deformation signals due to stress dissipation during friction and slip of yarns within the textiles. They are optimized for mechanical adaptability and adhesive capability. In this work, the stitch configurations of knitted structure are adjusted to optimize the energy dissipation ratio during deformation and waveform fitting performance. These electric‐mechanical results enabled the selection of the most suitable knitted structure for the clinical diagnosis. On the other hand, the sensor's adhesion is optimized with respect to electrical‐force‐strain coupling and energy transfer efficiency at the interface between skin and sensor. The balance between the storage modulus and loss modulus are adjusted via the crosslinking degree of the polyacrylamide (PAAm) hydrogel network. As a result, the optimized knitted sensor enables stable collection of pulse waveforms from the radial and dorsalis pedis arteries. In human patient evaluations, the knitting‐based strain sensor can distinguish patients with different potential CVD risks through extracted characteristic indicators.

Vascular dementia (VaD) is a syndrome of cognitive dysfunction caused by cerebrovascular damage. At present, VaD is mainly prevented by controlling vascular risk factors clinically, while there has been limited progress in therapies directly targeting its pathological mechanism. Mitochondrial dysfunction plays a key role in the pathogenesis of VaD, but there are no drugs to improve VaD by regulating mitochondrial function in clinical practice. In this study, semaglutide was used as an intervention therapy and results showed that semaglutide could regulate the balance of mitochondrial dynamics and mitophagy by activating the phosphatidylinositol 3‐kinase/protein kinase B signaling pathway, adjust the phenotype of glial cells from the proinflammatory states to the anti‐inflammatory states, and improve cognitive dysfunction. This study identifies a therapeutic way of linking semaglutide to hippocampal neuronal protection, reduction of pathology, and restoration of cognitive function, with important implications for the treatment of VaD.