Peripheral nerve injury (PNI) caused by trauma, chronic disease and other factors may lead to partial or complete loss of sensory, motor and autonomic functions, as well as neuropathic pain. Biological activities are always accompanied by mechanical stimulation, and biomechanical microenvironmental homeostasis plays a complicated role in tissue repair and regeneration. Recent studies have focused on the effects of biomechanical microenvironment on peripheral nervous system development and function maintenance, as well as neural regrowth following PNI. For example, biomechanical factors-induced cluster gene expression changes contribute to formation of peripheral nerve structure and maintenance of physiological function. In addition, extracellular matrix and cell responses to biomechanical microenvironment alterations after PNI directly trigger a series of cascades for the well-organized peripheral nerve regeneration (PNR) process, where cell adhesion molecules, cytoskeletons and mechanically gated ion channels serve as mechanosensitive units, mechanical effector including focal adhesion kinase (FAK) and yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) as mechanotransduction elements. With the rapid development of tissue engineering techniques, a substantial number of PNR strategies such as aligned nerve guidance conduits, three-dimensional topological designs and piezoelectric scaffolds emerge expected to improve the neural biomechanical microenvironment in case of PNI. These tissue engineering nerve grafts display optimized mechanical properties and outstanding mechanomodulatory effects, but a few bottlenecks restrict their application scenes. In this review, the current understanding in biomechanical microenvironment homeostasis associated with peripheral nerve function and PNR is integrated, where we proposed the importance of balances of mechanosensitive elements, cytoskeletal structures, mechanotransduction cascades, and extracellular matrix components; a wide variety of promising tissue engineering strategies based on biomechanical modulation are introduced with some suggestions and prospects for future directions.

Low capacitance and sluggish kinetics of positive and negative electrode materials are two main obstacles that restrict the electrochemical performance of flexible asymmetric supercapacitors (ASCs). In this work, an effective metal–organic framework (MOF)-derived approach is proposed to construct high-performance positive and negative electrode materials with a core–shell heterostructure. The binary MOF arrays are converted to zinc–cobalt sulfide nanosheet scaffolds with excellent conductivity and a ductile structure, which can offer an electrically and ionically conductive 3D continuous network for the growth of active materials. Based on this platform, the originally built Ni(OH)₂@ZnCoS-NSs are validated to be a highly capacitive positive electrode (8.1 F cm⁻² at 3 mA cm⁻², i.e., 2730 F g⁻¹), matching well with the similarly constructed VN@ZnCoS-NS negative electrode (1.35 F cm⁻² at 3 mA cm⁻²). Benefiting from the rationally engineered electrodes, the assembled ASC device can exhibit ultrahigh energy density (75 W h kg⁻¹ at a power density of 0.4 kW kg⁻¹), stable electrochemical stability (82% capacitance retention even after 10 000 cycles), and excellent flexibility (92% capacitance retention after bending 4000 times). This study demonstrates an attractive strategy for the rational design of high-performance heterostructure electrodes by exploiting the compositional and structural versatility of 2D MOF arrays.

As one of the most promising candidates for supercapacitor electrodes, vanadium pentoxide (V₂O₅) usually suffers from poor electronic conductivity and small ionic diffusivity.