Macrophage migration inhibitory factor facilitates the therapeutic efficacy of mesenchymal stem cells derived exosomes in acute myocardial infarction through upregulating miR-133a-3p.
Wenwu ZhuLing SunPengcheng ZhaoYaowu LiuJian ZhangYuelin ZhangYimei HongYeqian ZhuYao LuWei ZhaoXinguang ChenFeng-Xiang ZhangPublished in: Journal of nanobiotechnology (2021)
MIF-Exo can provide cardioprotective effects by promoting angiogenesis, inhibiting apoptosis, reducing fibrosis, and preserving heart function in vitro and in vivo. The mechanism in the biological activities of MIF-Exo involves miR-133a-3p and the downstream AKT signaling pathway.
Keyphrases
- signaling pathway
- mesenchymal stem cells
- acute myocardial infarction
- pi k akt
- cell cycle arrest
- umbilical cord
- induced apoptosis
- epithelial mesenchymal transition
- oxidative stress
- bone marrow
- endoplasmic reticulum stress
- heart failure
- endothelial cells
- stem cells
- left ventricular
- percutaneous coronary intervention
- adipose tissue
- cell death
- vascular endothelial growth factor
- cell proliferation
- cell therapy
- atrial fibrillation
- coronary artery disease
- liver fibrosis