Table 2.

The beneficial effects of Mitochondrial fission inhibition following ischaemia/reperfusion injury in ex vivo studies

Study model	Methods	Major finding		Interpretation	Ref
		Ischaemia/reperfusion injury	Mitochondrial fission inhibition
• Male C6/Black mice	• Langendorff‐perfused heart, I/R: 30/60 min. • Pretreated with →Dynasore: 1 µM	• ↑ LVEDP • ↑ Infarct size • ↑ cTnI	Dynasore • ↓ LVEDP • ↓ Infarct size • ↓ cTnI	Drp1 inhibition can limit cardiac damage through reducing myocardial infarct size, and cTnI and improving LV function.	32
• Male Wistar rats	• Langendorff‐perfused heart, I/R: 30/120 min. • Pretreated for 10 min. with P110: 1 µM	• ↑ Mitochondrial fission • ↓ Mitochondrial size • ↑ Mitochondrial Drp1 • ↑ Infarct size • ↑ ROS • ↓ ATP • ↑ Cleaved caspase 3	P110 • ↑ Mitochondrial elongation • ↓ Mitochondrial Drp1 • ↓ Infarct size • ↓ ROS • ↑ ATP • ↓ Cleaved caspase 3	Drp1 inhibitor restored mitochondrial functions, mitochondrial dynamics leading to decrease infarct size.	12
• Male Sprague‐Dawley rat	• Langendorff‐perfused heart, I/R: 30/20 min. • Pretreated for 10 min. with →Mdivi‐1: 5 µM →TH: 30oc →FK506: 0.3 µM	• ↓ p‐Drp1 Ser637 • ↑ Mitochondrial Drp1 • ↓ Systolic pressure • ↑ Diastolic pressure • ↑ End diastolic pressure • ↓ Developed pressure	Mdivi‐1, TH and FK506 • ↑ p‐Drp1 S637 • ↓ Mitochondrial Drp1 • ↓ Diastolic pressure • ↓ End diastolic pressure • ↑ Developed pressure	Drp1 inhibition improved myocardial function following I/R by increased OCR, reduced mitochondrial fission and improved cardiac function.	11

ATP: Adenosine triphosphate; cTnI: cardiac troponin I; Drp1: Dynamin‐related protein‐1; Dynasore: A small noncompetitive dynamin GTPase inhibitor; FK506: Calcineurin inhibitor; I/R: Ischaemia/Reperfusion; LVEDP: Left ventricular end systolic pressure; Mdivi‐1: Mitochondrial Division Inhibitor 1; p: Phosphorylation; P110: A selective inhibited the interaction of fission proteins Fis1/Drp1; ROS: Reactive oxygen species; TH: Therapeutic hypothermia.