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. 2024 Jan;19(1):6–13. doi: 10.18502/jthc.v19i1.15531

Table 2.

Involved miRNAs in endothelial dysfunction

MiRNA Disease Target Inflammation/Oxidative Stress Mechanism Effect on LIF Ref







MicroRNA-223-3p AMI NLRP-3 Anti-inflammatory Reducing the secretion of IL-1β Suppressing LIF expression (70, 81)
MicroRNA-146a MI Target IRAK1 & TRAF-6 Anti-inflammatory Attenuating NFκB activation and inflammatory cytokine production by suppressing IRAK-1 and TRAF-6 Inhibiting the expression of LIF (82, 83)
MicroRNA-21 MI KBTBD-7 gene Anti-inflammatory Promoting the activation of p38 and NFκB signaling by interacting with MKK3/6 LIF induces the expression of microRNA-21 (miR-21). (84, 85)
MicroRNA-125a Atherosclero-sis ET-1 Anti-inflammatory Suppressing oxLDL and inducing ET-1 expression MicroRNA 125a can induce the LIF receptor. (86, 87)
MicoRNA-146a Atherosclero-sis NOX-4 Anti-Inflammation Inhibiting the activation of TLR4-dependent signaling pathway Inhibit the expression of LIF (82, 88)
MicroRNA-141 Atherosclero-sis PAPP-A Inflammation Inhibiting the vascular smooth muscle cell proliferation LIF can induce the production of microRNA-21. (89, 90)

AMI, Acute myocardial infarction; NLRP3, NOD-, LRR- and pyrin domain-containing protein 3; MI, Myocardial infarction; IRAK1, Interleukin-1 receptor-associated kinase 1; TRAF-6, TNF receptor-associated factor-6; NFκB, Nuclear factor-kB; ET-1, Endothelin-1; oxLDL, Oxidized LDL; TLR-4, Toll-like receptor-4; PAPP-A, pregnancy-associated plasma protein-A