Table 1 The main findings of this article

CMs

The imbalance of Bax / Bcl2 ratio leads to the permeability of the mitochondrial outer membrane.

Some studies have focused on how Bax and Bcl2 change and maintain dynamic balance to protect cardiomyocytes.

[16,17,18,19,20,21,22,23,24]

The opening of the mPTP is the prerequisite of the integrity of IMM and plays a decisive role in releasing

mitochondrial apoptotic proteins. Studying its opening can reduce mitochondrial apoptosis and protect cardiomyocytes.

[27,28,29,30,31]

Mitochondrial apoptotic proteins (e.g. Cyt-C, caspase-3, caspase- 9) are increased in I/R injury,

and the death of CMs can be reduced by inhibiting the increase of these proteins.

[33,34,35]

Mitochondrial morphological changes play an important role in mitochondrial apoptosis. Inhibition

of excessive mitochondrial fission and appropriate increase of mitophagy can reduce mitochondrial apoptosis.

[37, 38, 39, 41–42]

ECs

Increased levels of ROS, elevated intracellular Ca²⁺, and decreased NO bioavailability lead to altered MMP,

disruption of the balance between anti-apoptotic and pro-apoptotic proteins, the opening of the mPTP,

and mitochondrial swelling and deformation; all of these initiate apoptosis via the mitochondrial pathway

[6, 44, 49]

[54–55]

The decrease in EC membrane stability leads to the release of mitochondrial-related apoptotic proteins,

which leads to mitochondrial apoptosis.

[56,57,58,59]

Although the number of mitochondria in ECs is small, they are of great significance. Abnormal mitochondrial morphology can lead to mitochondrial apoptosis.

[60,61,62,63]

VSMCs

The NO signaling pathway is important. NO preconditioning can inhibit Bcl-2/Bax/Apaf-1/caspase-3 mitochondrial apoptotic pathway.

[64]

CFs

CFs mainly play a repair and cardiac remodeling role during myocardial I/R, therefore,

inhibiting mitochondrial apoptosis can promote fibrosis.

[66,67,68,69,70]

MSCs

The core mechanism of action of MSCs involves the PI3K/Akt signaling pathway.

[11, 71,72,73]