Loss of SNORA73 makes cell metabolism reprogrammed and has a protective effect on steatohepatitis

Dyslipidemia and the resulting lipotoxicity are pathological features of metabolic syndrome and type 2 diabetes

Here, the authors demonstrated that the destruction of the H/ACA SNORA73 box small nucleolar RNA encoded in the small nucleolar RNA host gene 3 (Snhg3) resulted in the resistance of cultured cells to lipid-induced cell death and general oxidative stress

In a state of overnutrition, lipid overload will exceed the ability of adipose tissue to store triglycerides and the ability of non-fat tissue to metabolize fatty acids

The characteristic of lipotoxicity is that the stress response pathway is activated, which is caused by the physiological pathway that oversupply substrates for lipid utilization

Both endoplasmic reticulum stress and mitochondrial dysfunction can lead to the production of reactive oxygen species (ROS), which overwhelm the endogenous antioxidant mechanism

SNORA73 gene knockout can improve steatohepatitis

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Genetic screening confirmed the role of SNORA73 in regulating cell response to lipotoxicity and oxidative stress

In vivo and in vitro studies have shown that the loss of SNORA73 leads to metabolic rearrangement and elimination of lipotoxicity, revealing the way snoRNAs regulate cell metabolism and metabolic stress

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references

Arthur C Sletten et al.

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