At present, cardiovascular and cerebrovascular diseases seriously threaten human life and health, and the development of nanodrug delivery systems has brought about a turnaround for traditional drug treatments, with nanoparticles being precisely targeted to improve bioavailability. In addition, surface modification of nanoparticles can prolong blood circulation time and enhance targeting ability. The application of cell membrane-coated nanoparticles further improves their biocompatibility and active targeting ability, providing new hope for the treatment of cardiovascular and cerebrovascular diseases. In recent years, various types of cell membrane biomimetic nanoparticles have gradually attracted increasing attention due to their unique advantages. However, the single-cell membrane has several limitations because a single functional property cannot fully meet the requirements of cardiovascular and cerebrovascular disease treatment. Hybrid cell membranes integrate the advantages of multiple biological membranes and have become an emerging research hotspot. This review summarizes the application of single-cell membrane biomimetic nanoparticles in the treatment of cardiovascular and cerebrovascular diseases and discusses the advantages, challenges and future development of biomimetic nanoparticles. We propose that the fusion of multiple membranes may be a reasonable trend in the future to provide some ideas and directions for the treatment of cardiovascular and cerebrovascular diseases.

Background and Purpose: The transcription factor B cell lymphoma 6 (BCL6) is an oncogenic driver of diffuse large B cell lymphoma (DLBCL). Blocking the protein-protein interactions of BCL6 and its corepressors has been proposed as an effective approach for the treatment of DLBCL. However, BCL6 inhibitors with excellent drug-like properties are rare. Hence, the development of BCL6 inhibitors is worth pursuing. Experimental Approach: We screened our internal chemical library by luciferase reporter assay and Homogenous Time Resolved Fluorescence (HTRF) assay and a small molecule compound named WK500B was identified. The binding affinity between WK500B and BCL6 was evaluated by surface plasmon resonance (SPR) assay and the binding mode of WK500B and BCL6 was predicted by molecular docking. The function evaluation and anti-cancer activity of WK500B was detected by immunofluorescence assay, Real-Time Quantitative PCR, cell proliferation assay, cell cycle assay, cell apoptosis assay, enzyme-linked immunosorbent assay (ELISA) and animal models. Key Results: WK500B engaged BCL6 inside cells, blocked BCL6 repression complexes, reactivated BCL6 target genes, killed DLBCL cells and caused apoptosis as well as cell cycle arrest. In animal models, WK500B inhibited germinal centre (GC) formation and DLBCL tumor growth without toxic and side effects. Moreover, WK500B showed favourable pharmacokinetics and presented superior druggability compared to other BCL6 inhibitors. Conclusions and Implications: WK500B showed strong efficacy and favourable pharmacokinetics and presented superior druggability compared to other BCL6 inhibitors. So, WK500B is a promising candidate that could be developed as an effective orally available therapeutic agent for DLBCL.