Cerebral ischemic stroke (CIS) is a severe cerebrovascular disease that poses numerous challenges in diagnosis and treatment, primarily attributed to blood-brain barrier (BBB) constraints and inherent drug targeting limitations. Biomimetic membrane nanotechnology, as an emerging therapeutic approach, offers a novel therapeutic strategy by emulating biological membrane structures and functions. This review comprehensively examines biomimetic nanomedicines (BMNPs) in CIS management, encompassing preparation methodologies, material characterization, and specific diagnostic/therapeutic applications. We discussed in detail various types of biomimetic nano-materials such as conventional extracellular membranes, bacterial outer membranes, and virus-like particles, and explore their capacity in enhancing BBB penetration, improving target specificity, and evading immune clearance. Current challenges regarding biosafety profiles, manufacturing quality control, targeted modification precision, and controlled drug release kinetics are delineated in this review. Looking to the future, advancing synergies between nanotechnology and biomedicine hold significant promise for optimizing CIS theranostics and expanding clinical treatment modalities.

Correction on: Long Y, Zou Z, Wu Y, Feng H, Chen T, Yang Z, Jian X, Yin Y and Li X (2025) The original version of this article has been updated.

Ultrahigh dose-rate radiotherapy (FLASH-RT) represents a rapidly emerging radiotherapy modality with improved normal tissue protection. However, tumor radioresistance remains a major obstacle limiting its clinical potential. To address this, we developed a novel redox-responsive, PROTAC-based nanoplatform (APF) formed by the self-assembly of folate-conjugated PEG₂₀₀₀–ARV-771 (FA-PEG₂₀₀₀-ARV-771). Following FA-mediated targeting and endocytic uptake by tumor cells, APF nanoparticles underwent glutathione-triggered cleavage in the reductive tumor microenvironment, releasing ARV-771 which promoted the proteasomal degradation of BRD4. The reduction of BRD4 disrupted the BRD4-c-Myc-RAD51AP1 signaling pathway and damaged the DNA repair pathway that resulting in a significant sensitizing effect of FLASH radiotherapy using Petal Accelerator platform. Both in vitro and in vivo experiments demonstrated that APF-assisted FLASH-RT markedly induced tumor cell apoptosis and necrosis, effectively inhibiting the malignant progression of tumors. Additionally, APF significantly enhanced FLASH-RT-induced tumor cell killing by promoting intracellular reactive oxygen species (ROS) generation and exacerbating DNA double-strand breaks. Transcriptomic analysis further revealed that APF-mediated BRD4 degradation suppressed key DNA repair-related genes. As a result, the APF@FLASH-RT combination achieved superior tumor inhibition in vivo with minimal systemic toxicity. This work provides a promising nanomedicine strategy for enhancing FLASH radiotherapy efficacy through targeted protein degradation.