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Research Spotlight | CELL: circRNA SCAR Alleviates NASH via Reducing mROS Output


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.

Congratulations to researcher for publishing the latest articles in the top-level journal "Cell". It is a great honor for Elabscience's products to contribute to this great scientific research achievement. Elabscience is determined to be strict with itself and be the most loyal partner of scientific research scholars!

Fundamental Information

Title: Targeting Mitochondria-Located circRNA SCAR Alleviates NASH via Reducing mROS Output

Journal: Cell


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:

Cat. No


Detection target


Tested sample



Human IL-1β


Cell culture medium



Human TNF-α


Cell culture medium



Human IL-8


Cell culture medium

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.


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)


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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