Fig. 9: Schematic illustration of MAVS’ role in MIRI. | Nature Communications

Fig. 9: Schematic illustration of MAVS’ role in MIRI.

From: Myocardial mitochondrial antiviral signaling protein promotes heart Ischemia-reperfusion injury via RIG-I signaling in mice

Fig. 9

MIRI-induced reactive oxygen species (ROS) activates the RIG-I signaling cascade - at least in part - by RNA generated during myocardial death, in which MAVS plays the role of a hub to regulate downstream signaling: MAVS recruits and interacts with transforming growth factor-β-activated kinase 1 (TAK1) and tumor necrosis factor-associated factor family 6 (TRAF6), and participates in the mitogen-activated protein kinase/JNK signaling pathway, which triggers apoptosis-related pathways that induce cardiomyocyte apoptosis, immune cell infiltration and adverse ventricular remodeling such as increased fibrosis and impaired angiogenesis in vivo. MAVS deficiency prevents cardiomyocyte apoptosis and reduces immune cell infiltration and fibrosis, while promoting angiogenesis. JNK inhibition protects against MIRI. The graphics were generated with BioRender (https://app.biorender.com).

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