Background
Type I acute myocardial infarction (T1MI) has a very high morbidity and mortality rate. The role of thrombus-derived exosomes (TEs) in T1MI is unclear.
Conclusions
We demonstrate that TEs as a potential target and research direction for the treatment of heart failure after T1MI. TEs may regulate ferroptosis and autophagy in thrombus-adjacent cells through the enrichment of certain lncRNAs.
Methods
The objective of this study was to identify the optimal thrombolytic drug and concentration for extracting TEs. To this end, a series of time and concentration combinations were tested. Subsequently, the effect of TEs on thrombus-adjacent cells was investigated. Finally, we conducted lncRNA microarray analysis on the extracted TEs (GSE213115).
Results
TEs has been demonstrated to promote necrosis, autophagy, and ferroptosis of human cardiomyocytes, while inhibiting the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Furthermore, TEs can stimulate the proliferation and migration of smooth muscle cells, and induce a transformation from a contractile to a secretory phenotype. Bioinformatics analysis revealed that five lncRNAs, AC068418.2, AC010186.3, AL031430.1, AC121333.1, and AL136526.1, exhibited significant differential expression in TE and regulated cell autophagy and ferroptosis by directly binding to TP53, TP63, and RELA, respectively. Conclusions: We demonstrate that TEs as a potential target and research direction for the treatment of heart failure after T1MI. TEs may regulate ferroptosis and autophagy in thrombus-adjacent cells through the enrichment of certain lncRNAs.