MiR-98-5p promotes ischemia/reperfusion-induced microvascular dysfunction by targeting NGF and is a potential...

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• Biomarker Discovery

Background:

• ST-segment elevation myocardial infarction (STEMI) treatment involves primary percutaneous coronary intervention (pPCI).
• Microvascular reperfusion is critical for outcomes post-pPCI.
• The role of microRNAs in ischemia/reperfusion (I/R) injury remains an active area of research.

Purpose of the Study:

• To investigate the association between serum miR-98-5p levels and microvascular reperfusion indices in STEMI patients undergoing pPCI.
• To elucidate the underlying mechanisms of miR-98-5p in promoting I/R injury.

Main Methods:

• Serum miR-98-5p levels were quantified in 171 STEMI patients (no-reflow vs. reflow groups).
• In vitro studies assessed miR-98-5p, nerve growth factor (NGF), and transient receptor potential vanilloid 1 (TRPV1) in human coronary endothelial cells under hypoxia/reoxygenation (H/R).
• In vivo studies evaluated the effect of antagomir-98-5p on myocardial I/R-induced microvascular dysfunction in a rat model.

Main Results:

• Elevated serum miR-98-5p levels were linked to poorer microvascular reperfusion.
• H/R significantly increased miR-98-5p in cultured endothelial cells.
• NGF was identified as a direct target of miR-98-5p.
• Antagomir-98-5p treatment ameliorated microvascular dysfunction and modulated NGF and TRPV1 expression in vivo.

Conclusions:

• MiR-98-5p exacerbates microvascular dysfunction by targeting the NGF-TRPV1 axis.
• Serum miR-98-5p shows promise as a biomarker for assessing microvascular reperfusion after STEMI.