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In current studies, the mechanisms involved in UA induced cardiomyocytic injury include ROS/CaMKII/Parkin pathway (Zhang et al., 2020), and calpain-1 and endoplasmic reticulum stress (Yan et al., 2018)
The low membrane fluidity facilitates the formation of PAQR-2/IGLR-2 complex that presumably sends signals to its downstream effectors, NHR-49, MDT-15, or SBP-1, to promote fatty acid desaturation [112]
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This relationship has been demonstrated in experimental animal models and observational human research [73, 74]
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