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miR-340-5p alleviates oxidative stress injury by targeting MyD88 in sepsis-induced cardiomyopathy

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These findings not only reveal how specific genetic variations increase the risk of OA by affecting the biological functions of chondrocytes and the integrity of joint tissue but also point to new directions for research to further understand how these variations influence the development and progression of the disease

Further studies demonstrated that growth arrest-specific transcript 5 (GAS5) could act as a molecular sponge for miR-455-5p and regulate miR-455-5p/PTEN expression to counteract cisplatin-induced apoptosis and ROS production (Wu et al., 2024)

[28] reported that in early Th17 differentiation, H3K4me1 is deposited at Th17-related gene regulatory regions by specific histone methyltransferases, priming enhancers for subsequent binding by RORt