|
| Model | Effector | Target | Activity in MIRI | Ref. |
|
| Mouse | Tregs | Epicardial YAP/TAZ | The novel Hippo signaling effectors YAP/TAZ within epicardial can drive the immune chemokine target IFN-γ of Tregs to the injured myocardium and function as cardioprotectors post-AMI. | [93] |
| CD39 of Tregs | Unknown | Attenuates cardiomyocyte apoptosis and reduces neutrophil infiltration. | [92] |
| Key secreted proteins of Tregs | Unknown | Tregs function in a paracrine manner to promote cardiomyocyte proliferation for cardioprotection after AMI. The six secreted proteins including Cst7, Tnfsf11, Il33, Fgl2, Matn2, and Igf2 may be responsible. | [94] |
| IL-2/Anti-IL-2 mAb complex (IL-2C) | Unknown | IL-2C from the spleen and heart might selectively proliferate cardioprotective Tregs. | [95] |
| N,N-dimethylsphingosine (DMS) | IL-10, TGFβ | DMS applied during early AMI in vivo may be protective against MIRI by recruiting Tregs via the PI3K/Akt pathway. | [96] |
| S1P/FTY720 | CCL7, MMP-2 and IL-6 | FTY720 can reduce immune B cells and its associated chemokine CCL7 and suppress MMP-2 and IL-6 in order to prevent the heart from severe cardiac inflammation and immune responses. | [102] |
| TRAF3IP2 (previously known as CIKS or Act1) | NF-κB, JNK, p38 MAPK | Traf3ip2 gene deletion mediates an overall cardioprotective effects. | [104, 105] |
| IL-21 | Akt, NF-κB, p38MAPK | Increases chemokine expression by activating Akt/NF-κB signaling in cardiomyocytes and p38 MAPK/NF-κB signaling in cardiac fibroblasts. | [106] |
| Crk adaptor proteins | C3G, RAP1 | Crk adaptor proteins can mediate the initial steps of T-cells adhesion via its nSH3 domain binding to C3G, which is guanine-nucleotide exchange factors for the small GTPases RAP1. | [107] |
|
| Rat | S1P/FTY720 | (GSK)-3β, mPTP components | S1P receptor agonist FTY720 can inhibit GSK-3β and regulate opening of mPTP to be cardioprotective. | [101] |
|
| Human | Vildagliptin | TGF-β1 | Vildagliptin can recruit Tregs by overexpressing TGF-β1. | [97] |
|
