TABLE 1.

Summary of major studies investigating cardioprotection with pharmacological agents targeting mitochondrial fission proteins

Mitochondrial fission and fusion protein	Pharmacological agent	Animal acute myocardial IRI models	Cardioprotective effect	Comment
Drp1 16	Mdivi‐1, pre‐treatment	In vivo mouse heart	Reduced MI size and less fission
Drp1 67	Mdivi‐1, 15 min prior to reperfusion	In vivo mouse heart	Reduced MI size, less fission, improved mitochondrial function
Drp1 81	Mdivi‐1, alone or in nanoparticles at reperfusion	Ex vivo mouse heart	Both mdivi‐1 alone or in nanoparticles reduced MI size	Mdivi‐1 delivered by nanoparticles more cardioprotective.
Drp1 81	Mdivi‐1, alone or in nanoparticles at reperfusion	In vivo mouse heart	Mdivi‐1 only reduced MI size when delivered by nanoparticles	Mdivi‐1 delivered by nanoparticles more cardioprotective.
Drp1 80	Mdivi‐1, at reperfusion	In vivo closed‐chest pig heart	No reduction in MI size or change in mitochondrial morphology	Underpowered study.
Drp1 70	Dynasore, during reperfusion	Ex vivo mouse heart	Reduced MI size
hFis1‐Drp1 interaction 71	P110 in stabilization and during reperfusion	Ex vivo rat heart	Reduced MI size
hFis1‐Drp1 interaction 71	P110 at reperfusion	In vivo rat heart	Reduced MI size
Drp1 75	Drpitor1 and Drpitor1a pre‐treatment	Ex vivo rat heart	Improved right ventricle function, less fission and mitochondrial ROS production

Abbreviation: MI, myocardial infarct.