Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.

circ_0001084 acts as a competing endogenous RNA for miR-181c-5p, enhancing PTPN4 expression and inhibiting the TLR4/NF-κB signaling pathway. These findings offer insights into the molecular mechanisms of myocardial I/R injury and potential therapeutic targets in ischemic heart disease.

This study combined bioinformatic and experimental techniques to investigate myocardial injury. Gene expression data from the GEO database were analyzed, and HL-1 cardiomyocytes were used in a hypoxia/reoxygenation model to mimic reperfusion injury. Various molecular techniques have been applied to explore the underlying mechanisms, while statistical analyses have identified potential biomarkers and therapeutic targets.

This study revealed significant upregulation of miR-181c-5p in cardiomyocyte H/R injury models, which inversely affected PTPN4 expression and activated the TLR4/NF-κB signaling pathway. Overexpression of PTPN4 inhibited this pathway. Notably, circ_0001084 was identified as absorbing miR-181c-5p, reducing its interaction with PTPN4 and subsequent pathway activation. This suggests a novel therapeutic pathway for myocardial I/R injury treatment, highlighting the interplay between non-coding RNAs and cellular stress responses.