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Research Spotlight | CELL: circRNA SCAR Alleviates NASH via Reducing mROS Output
Source: Elabscience®Published: Feb 01,2024
The team of Professor Shicheng Su, Zhiliang Gao and Xiaoding Xu from Sun Yat-Sen University recently reported that A mitochondrial circRNA that is dysregulated in NAFLD patients’ liver fibroblasts directly binds and regulates the mitochondrial permeability transition pore to modulate mitochondrial metabolism and inflammation, providing a potential therapeutic angle.
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Fundamental Information
Title: Targeting Mitochondria-Located circRNA SCAR Alleviates NASH via Reducing mROS Output
Journal: Cell
IF:38.637(2019)
Institution of the first author: Sun Yat-Sen University, Guangzhou, China
Institution of the corresponding author: Sun Yat-Sen University, Guangzhou, China
Elabscience® Products Cited:
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PS: The IL-8 detection kit of Cat# E-EL-0048 cited in this paper has been optimized and the new Cat# is E-EL-H6008, we are sorry for the confusion.

SUMMARY
Mitochondria, which play central roles in immunometabolic diseases, have their own genome. However, the functions of mitochondria-located noncoding RNAs are largely unknown due to the absence of a specific delivery system.
By circular RNA (circRNA) expression profile analysis of liver fibroblasts from patients with nonalcoholic steatohepatitis (NASH), we observe that mitochondrial circRNAs account for a considerable fraction of downregulated circRNAs in NASH fibroblasts.
By constructing mitochondria-targeting nanoparticles, we observe that Steatohepatitis-associated circRNA ATP5B Regulator (SCAR), which is located in mitochondria, inhibits mitochondrial ROS (mROS) output and fibroblast activation. circRNA SCAR, mediated by PGC-1a, binds to ATP5B and shuts down mPTP by blocking CypD-mPTP interaction. Lipid overload inhibits PGC-1a by endoplasmic reticulum (ER) stress-induced CHOP.
In vivo, targeting circRNA SCAR alleviates high fat diet-induced cirrhosis and insulin resistance. Clinically, circRNA SCAR is associated with steatosis- to-NASH progression. Collectively, we identify a mitochondrial circRNA that drives metaflammation and serves as a therapeutic target for NASH.
Scheme of mitochondria-targeting nanoparticles (mito-NP)

Highlights
1. Mitochondria-located circRNA SCAR inhibits mROS output and fibroblast activation.
2. circRNA SCAR shuts down mPTP by binding to ATP5B.
3. Lipid-induced ER stress impairs PGC-1a-mediated circRNA SCAR expression.
4. Mitochondria-specific delivery of circRNA SCAR alleviates metaflammation in vivo.
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