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DNA materials have emerged as potential nanocarriers for targeted cancer therapy to precisely deliver cargos with specific purposes. The short half‐life and low bioavailability of DNA materials due to their interception by the reticuloendothelial system and blood clearance further limit their clinical translation. This study employs an HER2‐targeted DNA‐aptamer‐modified DNA tetrahedron (HApt‐tFNA) as a drug delivery system, and combines maytansine (DM1) to develop the HApt‐DNA tetrahedron/DM1 conjugate (HApt‐tFNA@DM1, HTD, HApDC) for targeted therapy of HER2‐positive cancer. To optimize the pharmacokinetics and tumor‐aggregation of HTD, a biomimetic camouflage is applied to embed HTD. The biomimetic camouflage is constructed by merging the erythrocyte membrane with pH‐responsive functionalized synthetic liposomes, thus with excellent performance of drug delivery and tumor‐stimulated drug release. The hybrid erythrosome‐based nanoparticles show better inhibition of HER2‐positive cancer than other drug formulations and exhibit superior biosafety. With the strengths of precise delivery, increased drug loading, sensitive tumor probing, and prolonged circulation time, the HApDC represents a promising nanomedicine to treat HER2‐positive tumors. Notably, this study developsa dual‐targeting nanoparticle by combining pH‐sensitive camouflage and HApDC, initiating an important step toward the development and application of DNA‐based medicine and biomimetic cell membrane materials in cancer treatment and other potential biological applications.

Denervation induces skeletal muscle atrophy, accompanied by complex biochemical and physiological changes, with potentially devastating outcomes even an increased mortality. Currently, however, there remains a paucity of effective strategies to treat skeletal muscle atrophy. Therefore, it is required to understand the molecular mechanisms of skeletal muscle atrophy and formulate new treatment strategies. In this study, we investigated the transcriptional profile of denervated skeletal muscle after peripheral nerve injury in rats. The cDNA microarray analysis showed that a huge number of genes in tibialis anterior (TA) muscles were differentially expressed at different times after sciatic nerve transection. Notably, the 24 h of denervation might be a critical time point for triggering TA muscle atrophy. According to the data from self-organizing map (SOM), Pearson correlation heatmap, principal component analysis (PCA), and hierarchical clustering analysis, three nodal transitions in gene expression profile of the denervated TA muscle might partition the period of 0.25 h–28 days post nerve injury into four distinct transcriptional phases. Moreover, the four transcriptional phases were designated as “oxidative stress stage”, “inflammation stage”, “atrophy stage” and “atrophic fibrosis stage”, respectively, which was concluded from Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene ontology (GO) analyses at each transcriptional phase. Importantly, the differentially expressed genes at 24 h post sciatic nerve transection seemed to be mainly involved in inflammation, which might be a critical process in denervation-induced muscle atrophy. Overall, our study would contribute to the understanding of molecular aspects of denervation-induced muscle atrophy, and may also provide a new insight into the time window for targeted therapy.