Fig. 1 Physicochemical characterization of GO-Au/CS composite scaffolds[28] (a-d) SEM images of (a) CS, (b) CS/0.1% GO-Au, (c) CS/0.25% GO-Au, and (d) CS/0.5% GO-Au (scale bar is 500 µm); (e) XRD patterns and (f) FT-IR spectra of composite scaffolds at different concentrations

Fig. 2 Schematic diagrams on preparation and application of SiO2-Fe3O4 composite microspheres[33] (a) Schematic of treatment with SiO2-Fe3O4 composite microspheres; (b) Schematic synthesis of composite microspheres

Fig. 3 Overall effects and mechanism of ion therapy on MI treatment[39] (a) Mechanism of ion therapy; (b) Effect of silicon-enriched ion extract on the expression of gap junction associated Cx-43 in NRCMs under glucose/oxygen deprived conditions in vitro; (c) Effect of silicon-enriched ion extract on VEGF-mediated angiogenesis of NRCMs and HUVECs co-cultures under glucose/oxygen deprived conditions in vitro; (d) Effect of ion therapy on cardiac apoptosis in vivo post-MI. NRCMs: neonatal rat cardiomyocytes; VEGF: vascular endothelial growth factor

Fig. 4 Component of the PSi NP and its therapeutic effect on MI[44] (a) Schematic components of the PSi NP and overview of studies conducted in vitro and in vivo; (b) Single-photon emission computed tomography (SPECT/CT) image quantification of the standardized uptake values in the rat heart at different time after intravenous (i.v.) administration of NPs; (c) SPECT/CT images showing the biodistribution of the nanoparticles at 10 min after i.v. administration; (d) H&E stainings and autoradiograms of apical, basal, and medial rat heart sections; (e) Autoradiographic quantification of radioactivity in the endocardium (Endo) and epicardium (Epi) for Un-P-D-ANP and Un-P-D NPs; (f) Autoradiographic quantification of radioactivity in the Endo and Epi regions of the heart in the apical, medial, and basal sections in isoprenaline-induced MI and normal rat groups; (g) TEM image of Un-P-D-ANP NPs in the NP Endo region of a heart section; (h) Elemental composition of the selected area by EDX analysis showing the presence of the Si element. PSi, NP, Un-P-D-ANP, and Un-P-D denote porous silicon, nanoparticle, undecylenic acid-porous silicon-atrial natriuretic peptide, and undecylenic acid-porous silicon, respectively

Fig. 5 PCL/Fe3O4/PVDF composite piezoelectric myocardial patch promoting myocardial regeneration by rebuilding electrical signaling at the damaged myocardium[54] (a) Strategy of engineering cardiac constructs with synergistic mechanical/piezoelectric stimulation; (b) Engineered cardiac constructs with synergistic mechanical/piezoelectric stimulation preserving left ventricular function after acute MI in vivo

Fig. 6 Carbon-based materials promoting myocardial repair by reconstructing mechanical-electrical microenvironment[77-78,103] (a) Schematic diagram of preparation of elastic conductive myocardial patch with GPE and its application[77]; (b-d) MI, MI + PGS and MI + PGS-Gr1 group heart tissue images[77]; (e) Statistical results of infarct area[77]; (f) Ultrasound imaging being performed at 4 weeks post-MI to assess cardiac functionality[77]; (g) Assessment of left ventricular internal dimension in systole (LVIDs), LVID in diastole (LVIDd), fractional shortening (FS) and ejection fraction (EF) at 4 weeks post-MI[77]; (h) Scheme of application of soft and conductive PEG-MEL/HA-SH/GO hydrogel system[78]; (i) Schematics illustrating fabrication of rGO/silkA/R scaffolds and their application in restoring electrical integrity in infarcted myocardium[103]

Fig. 7 Zn2SiO4 bioceramic repairing myocardial injury by manipulating cell behaviors[105] (a) Schematic diagram of the Zn2SiO4 for treatment of MI; (b) Zn2SiO4 bioceramic extract preventing H2O2-induced oxidative stress and apoptosis in H9C2 cells; (c) Zn2SiO4 bioceramic extract promoting angiogenesis of MCAECs; (d) Intravenous injection of Zn2SiO4 bioceramic extract reversing ventricular remodeling after MI in mice, including improving the cardiac function and decreasing the infarct size and the fibrosis area

Fig. 8 Biological mechanism of SiO32- treating iDCM[109] SiO32- modulated multicellular differentiation and interactions via FOXO signaling pathway. SiO32- activated the FOXO1 signaling pathway in CD4+ T cells, leading to a significant reduction in their differentiation into Th17 cells. Concurrently, CS promoted FOXO3 expression in neutrophils and fibroblasts, thereby inhibiting their differentiation into NETs and myofibroblasts, respectively. This comprehensive and multi-cellular regulatory mechanism disrupted the harmful interactions between CD4+ T/Th17 cells and neutrophils/ fibroblasts, breaking the vicious cycle of myocardial inflammation and blocking the progression of fibrotic lesions post iDCM