Fig. 5. Drp1 C644S hetero knock-in mice fail to cardioprotective effects of GSSG after MI.

A Schematic illustration of CRISPR/Cas9-mediated gene editing for Dnm1l (Drp1). Drp1 C644S knock-in mice were generated by mutating Cys TGT codon at position 644 to Ser TCG codon. The sequences of gRNA and template DNA were shown. B Genome DNA sequencing identified Drp1^C644S(CS)/+ hetero knock-in mutation. C Experimental protocol. One week after myocardial infarction (MI), cardiac functions of Drp1^+/+ and Drp1^CS/+ were analyzed by echocardiography. Then, an osmotic pump filled with saline or GSSG (30 mg/kg/day) was implanted intraperitoneally, and cardiac functions were analyzed again after an additional 3 weeks. D–F Changes in ejection fraction (EF) D, fractional shortening (FS) E and end-diastolic volume (EDV) F in Drp1^+/+ or Drp1^CS/+ mice 1 week after MI. (n = 10 mice for Drp1^+/+ MI, n = 11 mice for Drp1^CS/+) G–I Effect of GSSG on EF G, FS H and heart weight (HW) / tibia length (TL) ratio I in Drp1^+/+ or Drp1^CS/+ mice 4 weeks after MI. (n = 6 mice for Drp1^CS/+ MI + GSSG, n = 5 for others). Data are shown as the means ± SEM. Significance was determined by one-way ANOVA followed by Tukey’s post-hoc test. Source data are provided as a Source Data file.