Fig. 4
- ID
- ZDB-FIG-250725-23
- Publication
- Deng et al., 2025 - Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects
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The knockdown of grem1a induced zebrafish heart dysplasia and dysfunction. A Diagram of grem1a knockdown through CRISPER interference using zebrafish zygotes. B The efficiency of grem1a knockdown at 48 hpf. C The morphological statistic of grem1a-knockdown zebrafish at 72 hpf. D Representative images of grem1a-knockdown zebrafish at 72 hpf with corresponding enlarged heart picture (n = 30). E Heart beat rate and F the thickness of ventricular myocardium of grem1a-knockdown zebrafish at 72 hpf. G Diagram of the zebrafish heart structure (up), representative fluorescent images of the end of diastole and the end of systole of grem1a-knockdown Tg(cmlc2;EGFP) line at 72 hpf (n = 15). V, ventricle. A, atrium. H Ejection fraction, I strove volume, J fractional area change and K fractional shortening of grem1a-knockdown zebrafish at 72 hpf. *, P < 0.05; **, P < 0.01; ****, P < 0.0001 vs control |