ArticleCell death discovery2022
HtrA2/Omi mitigates NAFLD in high-fat-fed mice by ameliorating mitochondrial dysfunction and restoring autophagic flux.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- An in vivo "turning model" reveals new RanBP9 interactions in lung macrophages.Cell death discovery · 2025Article
- Altered mitochondrial function: a clue therapeutic strategies between metabolic dysfunction-associated steatotic liver disease and chronic kidney disease?Frontiers in nutrition · 2025Review
- Quercetin: A Promising Candidate for the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Molecules (Basel, Switzerland) · 2024Review
- Gut microbial metabolites in MASLD: Implications of mitochondrial dysfunction in the pathogenesis and treatment.Hepatology communications · 2024Review
- Recent advances in age-related metabolic dysfunction-associated steatotic liver disease.World journal of gastroenterology · 2024Review
- Dysfunction of autophagy in high-fat diet-induced non-alcoholic fatty liver disease.Autophagy · 2024Review
- Zaluzanin C Alleviates Inflammation and Lipid Accumulation in Kupffer Cells and Hepatocytes by Regulating Mitochondrial ROS.Molecules (Basel, Switzerland) · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver metabolic syndrome which affects millions of people worldwide. Recently, improving mitochondrial function and autophagic ability have been proposed as a means to prevent NAFLD. It has been previously described that high-temperature requirement protein A2 (HtrA2/Omi) favors mitochondrial homeostasis and autophagy in hepatocytes. Thus, we explored the effects of HtrA2/Omi on regulating mitochondrial function and autophagy during NAFLD development. High-fat diet (HFD)-induced NAFLD in mice and free fatty acids (FFAs)-induced hepatocytes steatosis in vitro were established. Adeno-associated viruses (AAV) in vivo and plasmid in vitro were used to restore HtrA2/Omi expression. In this study, we reported that HtrA2/Omi expression considerably decreased in liver tissues from the HFD-induced NAFLD model and in L02 cells with FFA-treated. However, restoring HtrA2/Omi ameliorated hepatic steatosis, confirming by improved serum lipid profiles, glucose homeostasis, insulin resistance, histopathological lipid accumulation, and the gene expression related to lipid metabolism. Moreover, HtrA2/Omi also attenuated HFD-mediated mitochondrial dysfunction and autophagic blockage. TEM analysis revealed that liver mitochondrial structure and autophagosome formation were improved in hepatic HtrA2/Omi administration mice compared to HFD mice. And hepatic HtrA2/Omi overexpression enhanced mitochondrial fatty acid β-oxidation gene expression, elevated LC3II protein levels, induced LC3 puncta, and decreased SQSTM1/p62 protein levels. Furthermore, hepatic HtrA2/Omi increased respiratory exchange ratio and heat production in mice. Finally, HtrA2/Omi overexpression by plasmid significantly diminished lipid accumulation, mitochondrial dysfunction, and autophagic inhibition in FFA-treated L02 hepatocytes. Taken together, we demonstrated that HtrA2/Omi was a potential candidate for the treatment of NAFLD via improving mitochondrial functions, as well as restoring autophagic flux.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.