The brittleness of traditional ceramics severely limits their application progress in engineering. The multiscale structural design of organisms can solve this problem, but it still lacks sufficient research and attention. The underlined main feature is the multiscale hierarchical structures composed of basic nano–microstructure units arranged in order, which is currently impossible to achieve through artificial synthesis driven by high temperatures. This perspective aims to bridge the gap between biostructural materials and biomimetic ceramics, highlighting the relationship between bioinspired structures and interfacial interaction of structure densification in biomimetic ceramics. Therefore, we could accomplish densification and ceramic development at room temperature, consequently correlating the structure, properties, and functions of materials and accelerating the development of the next generation of advanced functional ceramics.

Human breast milk serves as a vital source of nutrition for infants, and it also plays a critical role in shaping the infant gut microbiota and establishing intestinal homeostasis. This process substantially impacts immune function, neurodevelopment, and overall health. The noninvasive nature of breast milk collection makes it an ethical and accessible area for research, positioning it as a key focus for future studies. These future directions include the identification of novel bacteria combination, the establishment of comprehensive databases on infant microbiota, and the use of computational models to predict interactions between breast milk components and the gut microbiome. Additionally, the creation of diverse biological models and the establishment of infant stool banks will further enhance understanding of host–microbiome interactions and support disease prevention strategies.

Circular RNAs (circRNAs) are differentially expressed in cardiac hypertrophy; however, the exact function and mechanisms during hypertrophy development are still unknown. Here, we explored the role of a newly discovered circRNA in the pathogenesis of myocardial hypertrophy. It was found that circ-0001283 promoted the progression of cardiac hypertrophy by interacting with myosin light chain 3 (MYL3) to inhibit the protein ubiquitination and enhance its protein expression, not by the competitive endogenous RNA mechanism. Further investigation demonstrated that the reduced hypertrophy induced by circ-0001283 knockdown was counteracted by overexpression of MYL3. Mechanistically, MYL3 facilitated myocardial hypertrophy by inducing autophagy in cells via PI3K/Akt/mTOR and ERK signaling pathways. In summary, circ-0001283 can bind directly to MYL3 and up-regulate its expression, thereby promoting autophagy to accelerate cardiac hypertrophy. Circ-0001283 may serve as a potential therapeutic target for cardiac hypertrophy.

Atherosclerosis (AS) is a chronic inflammatory condition influenced by glucose and lipid disorders, oxidative stress, and thrombosis, reflecting the complexity of its pathological process. The development of accurate experimental models that simulate human AS is essential for understanding its initiation and progression. This review summarizes the current AS research models and analyzes their specific application scenarios. We discuss tissue-engineered blood vessels (TEBVs) and vessels-on-a-chip (VoCs), which leverage tissue engineering and precise microenvironmental control to construct in vitro models that closely resemble the structure and function of human AS. Isolated vessel segments from live animals provide a valuable tool for investigating human AS due to their physiological similarity, controllability, and reproducibility. The review further outlines the construction of AS animal models through high-fat diets and gene-editing techniques, highlighting how immune-inflammatory responses, mechanical arterial injury, and hemodynamic changes accelerate model development. This comprehensive analysis highlights the potential of AS models to revolutionize theranostic applications in clinical translational research, paving the way for more personalized and effective treatments for AS in the near future.

The prevention of air pollution-related cardiopulmonary disorders has been largely overlooked despite its important burden. Extracellular vesicles (EVs) have shown great potential as carriers for drug delivery. However, the efficiency and effect of EVs derived from different sources on ambient fine particulate matter (PM2.5)-induced cardiopulmonary injury remain unknown. Using PM2.5-exposed cellular and mouse models, we investigated the prevention of air pollution-related cardiopulmonary injury via an innovative strategy based on EV delivery. By using a “2-step” method that combines bibliometric and bioinformatic analysis, we identified superoxide dismutase 2 (Sod2) as a potential target for PM2.5-induced injury. Sod2-overexpressing plasmid was constructed and loaded into human plasma-, bovine milk-, and fresh grape-derived EVs, ultimately obtaining modified nanoparticles including PEV^Sod2, MEV^Sod2, and GEV^Sod2, respectively. GEV^Sod2, especially its lyophilized GEV^Sod2 powder, exhibited superior protection against PM2.5-induced cardiopulmonary injury as compared to PEV^Sod2 and MEV^Sod2. High-sensitivity structured illumination microscopy imaging and immunoblotting showed that GEV^Sod2 powder treatment altered lysosome positioning by reducing Rab-7 expression. Our findings support the use of fruit-derived EVs as a preferred candidate for nucleic acid delivery and disease treatment, which may facilitate the translation of treatments for cardiopulmonary injuries.

Simulated microgravity (SMG) poses substantial challenges to astronaut health, particularly impacting osteoblast function and leading to disuse osteoporosis. This study investigates the adverse effects of SMG on osteoblasts, focusing on changes in mitochondrial dynamics and their consequent effects on cellular energy metabolism and mechanotransduction pathways. We discovered that SMG markedly reduced the expression of osteoblast differentiation markers and promoted mitochondrial fission, as indicated by an increase in punctate mitochondria, a decrease in mitochondrial length, and a reduction in cristae density. These mitochondrial alterations are linked to elevated reactive oxygen species levels, a decrease in ΔΨm, and a metabolic shift from oxidative phosphorylation to glycolysis, resulting in decreased adenosine triphosphate production, which are all indicative of mitochondrial dysfunction. Our results showed that treatment with mitochondrial division inhibitor-1 (mdivi-1), a mitochondrial fission inhibitor, effectively inhibited these SMG-induced effects, thereby maintaining mitochondrial structure and function and promoting osteoblast differentiation. Furthermore, SMG disrupted critical mechanotransduction processes, by affecting paxillin expression, the RhoA–ROCK–Myosin II pathway, and actin dynamics, which subsequently altered nuclear morphology and disrupted Yes-associated protein signaling. Notably, treatment with mdivi-1 prevented these disruptions in mechanotransduction pathways. Moreover, our study showed that SMG-induced chromatin remodeling and histone methylation, which are epigenetic barriers to osteogenic differentiation, can be reversed by targeting mitochondrial fission, further highlighting the significance of mitochondrial dynamics in osteoblast function in an SMG environment. Therefore, targeting mitochondrial fission emerges as a promising therapeutic strategy to alleviate osteoblast dysfunction under SMG conditions, providing novel approaches to maintain bone health during prolonged space missions and safeguard the astronaut well-being.

Macrophages are ubiquitous within the human body and serve pivotal roles in immune surveillance, inflammation, and tissue homeostasis. Phenotypic plasticity is a hallmark of macrophages, allowing their polarization into distinct phenotypes M1 (pro-inflammatory, anti-tumor) and M2 (anti-inflammatory, pro-tumor) in response to local microenvironmental cues. In tumor tissues, the polarization of tumor-associated macrophages profoundly shapes the tumor microenvironment, influencing tumor progression, immune evasion, and metastasis. Therefore, the ability to image and monitor macrophage polarization is essential for comprehending tumor biology and optimizing therapeutic strategies. With the rapid advancement of nanomedicine, a diverse array of nanoprobes has been engineered to specifically target tumor-associated macrophages, offering new avenues for noninvasive in vivo imaging and real-time monitoring of macrophage dynamics within the tumor microenvironment. This perspective highlights recent advancements in macrophage-targeting nanoprobes for imaging macrophage polarization both in vitro and in vivo. It also addresses the current challenges in the field, such as enhancing probe sensitivity, specificity, and biocompatibility, while outlining the future directions for the development of next-generation nanoprobes aimed at precision oncology.

Nano-/microrobots have been demonstrated as an efficient solution for environmental remediation. Their strength lies in their propulsion abilities that allow active “on-the-fly” operation, such as pollutant detection, capture, transport, degradation, and disruption. Another advantage is their versatility, which allows the engineering of highly functional solutions for a specific application. However, the latter advantage can bring complexity to applications; versatility in dimensionality, morphology, materials, surface decorations, and other modifications has a crucial effect on the resulting propulsion abilities, compatibility with the environment, and overall functionality. Synergy between morphology, materials, and surface decorations and its projection to the overall functionality is the object of nanoarchitectonics. Here, we scrutinize the engineering of nano-/microrobots with the eyes of nanoarchitectonics: we list general concepts that help to assess the synergy and limitations of individual procedures in the fabrication processes and their projection to the operation at the macroscale. The nanoarchitectonics of nano-/microrobots is approached from microscopic level, focusing on the dimensionality and morphology, through the nanoscopic level, evaluating the influence of the decoration with nanoparticles and quantum dots, and moving to the decorations on molecular and single-atomic level to allow very fine tuning of the resulting functionality. The presented review aims to lay general concepts and provide an overview of the engineering of functional advanced nano-/microrobot for environmental remediation procedures and beyond.

Excessive gonadotropin-releasing hormone (GnRH) is considered to be an initiating factor in the etiology of polycystic ovary syndrome (PCOS). GnRH neuronal axons terminate at the hypothalamic arcuate nucleus and median eminence, where tanycytes, specialized glial cells, have been proposed to modulate GnRH secretion through plasticity. However, the precise role of the “GnRH-tanycyte unit” during the pathological state of PCOS has not been thoroughly explored. In this study, we demonstrated the architecture and distribution of GnRH neurons and tanycytes. In PCOS-like mice, retracted tanycyte processes and dysregulated GnRH-tanycyte unit may create an environment conducive to the excessive secretion of GnRH and subsequent reproductive endocrine dysfunction. Mechanistically, excessive androgens impair hypothalamic neuroglial homeostasis by acting through the androgen receptor (AR) and its downstream target integrin β1 (Itgb1), thereby suppressing the FAK/TGF-βR1/Smad2 signaling pathway. Both selective deletion of AR and overexpression of Itgb1 in tanycytes counteracted the detrimental effects of androgens, alleviating endocrine dysfunction. Collectively, this study highlights the alterations in the GnRH-tanycyte unit mediated by androgen/AR/Itgb1 signaling and provides a novel perspective for developing therapies for hypothalamic hormone secretion disorders by maintaining solid neuroglial structures in the brain.