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Soft and stretchable electronics have emerged as highly promising tools for biomedical diagnosis and biological studies, as they interface intimately with the human body and other biological systems. Most stretchable electronic materials and devices, however, still have Young’s moduli orders of magnitude higher than soft bio-tissues, which limit their conformability and long-term biocompatibility. Here, we present a design strategy of soft interlayer for allowing the use of existing stretchable materials of relatively high moduli to versatilely realize stretchable devices with ultralow tissue-level moduli. We have demonstrated stretchable transistor arrays and active-matrix circuits with moduli below 10 kPa—over two orders of magnitude lower than the current state of the art. Benefiting from the increased conformability to irregular and dynamic surfaces, the ultrasoft device created with the soft interlayer design realizes electrophysiological recording on an isolated heart with high adaptability, spatial stability, and minimal influence on ventricle pressure. In vivo biocompatibility tests also demonstrate the benefit of suppressing foreign-body responses for long-term implantation. With its general applicability to diverse materials and devices, this soft-interlayer design overcomes the material-level limitation for imparting tissue-level softness to a variety of bioelectronic devices.

 

Macrophages are essential for skeletal muscle homeostasis, but how their dysregulation contributes to the development of fibrosis in muscle disease remains unclear. Here, we used single-cell transcriptomics to determine the molecular attributes of dystrophic and healthy muscle macrophages. We identified six clusters and unexpectedly found that none corresponded to traditional definitions of M1 or M2 macrophages. Rather, the predominant macrophage signature in dystrophic muscle was characterized by high expression of fibrotic factors, galectin-3 (gal-3) and osteopontin (Spp1). Spatial transcriptomics, computational inferences of intercellular communication, and in vitro assays indicated that macrophage-derived Spp1 regulates stromal progenitor differentiation. Gal-3⁺macrophages were chronically activated in dystrophic muscle, and adoptive transfer assays showed that the gal-3⁺phenotype was the dominant molecular program induced within the dystrophic milieu. Gal-3⁺macrophages were also elevated in multiple human myopathies. These studies advance our understanding of macrophages in muscular dystrophy by defining their transcriptional programs and revealSpp1as a major regulator of macrophage and stromal progenitor interactions.

 

A stretchable pressure sensor is a necessary tool for perceiving physical interactions that take place on soft/deformable skins present in human bodies, prosthetic limbs, or soft robots. However, all existing types of stretchable pressure sensors have an inherent limitation, which is the interference of stretching with pressure sensing accuracy. Here, we present a design for a highly stretchable and highly sensitive pressure sensor that can provide unaltered sensing performance under stretching, which is realized through the synergistic creations of an ionic capacitive sensing mechanism and a mechanically hierarchical microstructure. Via this optimized structure, our sensor exhibits 98% strain insensitivity up to 50% strain and a low pressure detection limit of 0.2 Pa. With the capability to provide all the desired characteristics for quantitative pressure sensing on a deformable surface, this sensor has been used to realize the accurate sensation of physical interactions on human or soft robotic skin.