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. 2026 Mar 14;24:495. doi: 10.1186/s12951-026-04274-9

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© The Author(s) 2026

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 3 — M1-Migs exert injurious effects primarily through guanylate binding protein-5 (GBP5). (A) Flowchart of quantitative proteomic sequencing (Astral-DIA) for M0-Migs and M1-Migs (n = 3). (B) Quantitative volcano plot demonstrating differentially expressed proteins between M0-Migs and M1-Migs, with GBP5 ranked fifth among upregulated proteins in M1-Migs/M0-Migs. (C) Heat map of differentially expressed proteins between M0-Migs and M1-Migs, with GBP5 highlighted with red rectangles. (D) Western blot analysis comparing the protein profiles of M0-Migs and M1-Migs with the same amount of total protein (n = 4). (E) Western blot comparison of GBP5 and migrasome-related protein expression between normal controls (NC) and MI groups. The quantitative results are presented as bar graphs (n = 6). (F) Immunofluorescence localization of GBP5 in M1-Migs. Scale bars = 10 μm (low magnification) and 5 μm (high magnification). Data are representative of three biologically independent experiments. (G) Echocardiographic comparison of left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and left ventricular end-diastolic volume (LVEDV) between groups (n = 6). (H) Masson’s trichrome staining for infarct area comparison. Scale bars = 0.500 mm (n = 6). (I) Triphenyltetrazolium chloride (TTC) staining demonstrating a significantly larger infarct area in the M1-Migs group than in the M1-Migs guanylate binding protein 5 knockdown (GBP5-KD) group. Scale bars = 1 cm (n = 6). (J) Hematoxylin and eosin (HE) staining to detect myocardial tissue injury in both groups. Scale bars = 50 μm (n = 6). K) Calcein/propidium iodide (PI) viability assay for HL-1 cell mortality under two treatments. Scale bars = 100 μm (n = 3). L) Cell Counting Kit-8 (CCK8) assay to assess HL-1 cell viability under two treatments (n = 3). Results were shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001. One-way or two-way ANOVA variance was applied for multivariate analysis. Unpaired t-tests were applied to compare two groups