The Tohoku journal of experimental medicine
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Tohoku J. Exp. Med. · Jan 2025
Plasma MiR-21-5p and MiRNA-93-5p Levels as Early Assessment Tools for In-Stent Restenosis Following Endovascular Stenting Treatment in Patients with Lower Extremity Atherosclerotic Disease.
In-stent restenosis (ISR) still remains a leading cause of failure of interventional therapy in patients with lower extremity atherosclerotic disease (LEAD). Sensitive and reliable biomarkers to predict ISR should be identified. This study aims to investigate predictive values of two microRNAs, miR-21-5p and miR-93-5p for ISR following endovascular stenting treatment. ⋯ The plasma levels of miR-21-5p and miR-93-5p at 14 days after surgery used alone or combination as a test to predict ISR occurrence 6 months after surgery produced an AUC of 0.845, 0.839, and 0.906, respectively. Multiple logistic regression analysis revealed the plasma levels of miR-21-5p and miR-93-5p at 14 days after surgery were risk factors for LEAD patients developing ISR at 6 months after surgery (P < 0.001). Our results suggest that plasma miR-21-5p and miR-93-5p levels at 14 days after surgery may serve as potential biomarkers for developing ISR following endovascular stenting treatment among LEAD patients.
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Tohoku J. Exp. Med. · Jan 2025
Long Noncoding RNA GAS5 Contributes to Mycoplasma Pneumoniae Pneumonia by Regulating NF-κB via MiR-29c/HMGB1 Axis.
Mycoplasma pneumoniae pneumonia (MPP) poses a major threat to pediatric health. Our previous study suggested that GAS5 level was elevated in the peripheral blood of MPP children. However, the mechanism by which GAS5 regulates lung inflammation Mycoplasma pneumoniae (MP) infection-induced remains unknown. ⋯ Ectopic expression of GAS5 counteracted the effect of miR-29c mimic, and miR-29c inhibitor counteracted the effect of HMGB1 knockdown. Furthermore, silencing of GAS5 significantly alleviated MPP-induced inflammation and pathological lung injury in the MPP mouse model. GAS5/miR-29c/HMGB1 is highly involved in inflammation and lung histopathological injury in MPP disease progression by regulating the NF-κB signaling pathway.