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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
MRPL44 regulates lipid metabolism in metabolic dysfunction-associated steatotic liver disease through BNIP3-mediated
Siqi Liu1, Lianggui Xiao2, Qiuchen Cheng1
1Institute of Digestive Disease, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Objective:
Mitophagy is a critical defense mechanism against metabolic dysfunction-associated steatotic liver disease. MRPL44, a mitochondrial ribosomal protein that regulates mitochondrial DNA-encoded gene expression, has not previously been linked to lipid metabolism.
Methods:
This study employed an oleic acid/palmitic acid induced HepG2 cell models and a high-fat diet fed mouse models, combined with lentivirus-mediated MRPL44 overexpression and mitophagy assays, to investigate the regulatory role of MRPL44 in the progression of metabolic dysfunction-associated steatotic liver disease.
Results:
Our findings demonstrated that MRPL44 alleviates lipid metabolic disorders induced by high-fat diet through the mitophagy pathway. Specifically, in oleic acid/palmitic acid-stimulated HepG2 cells, overexpression of MRPL44 reduced intracellular triglyceride accumulation and enhanced fatty acid oxidation. Moreover, liver-specific overexpression of MRPL44 in mice attenuated high-fat diet induced hepatic lipid deposition. Mechanistically, MRPL44 activated the BNIP3-dependent mitophagy pathway, promoted mitochondrial biogenesis, and mitigated mitochondrial damage, ultimately reducing lipid accumulation in hepatocytes.
Conclusion:
This study identifies MRPL44 as a novel regulator of lipid metabolism and a potential therapeutic target for metabolic dysfunction-associated steatotic liver disease.
Insights
Mitophagy combats metabolic dysfunction-associated steatotic liver disease. This study reveals MRPL44 protein alleviates liver fat buildup by enhancing mitophagy, offering a new therapeutic target.
Area of Science:
- Hepatology and metabolic disease research.
- Mitochondrial biology and cellular stress response.
Background:
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is linked to impaired mitophagy.
- The role of mitochondrial ribosomal protein 44 (MRPL44) in lipid metabolism was previously unknown.
Purpose of the Study:
- To investigate the role of MRPL44 in MASLD progression.
- To explore MRPL44's regulatory function in lipid metabolism and mitophagy.
Main Methods:
- Utilized HepG2 cell models with oleic/palmitic acid induction.
- Employed high-fat diet mouse models with lentivirus-mediated MRPL44 overexpression.
- Conducted mitophagy assays to assess MRPL44's impact.
Main Results:
- MRPL44 overexpression reduced triglyceride accumulation and enhanced fatty acid oxidation in HepG2 cells.
- Liver-specific MRPL44 overexpression in mice attenuated high-fat diet-induced hepatic lipid deposition.
- MRPL44 activated the BNIP3-dependent mitophagy pathway, promoting mitochondrial biogenesis and reducing lipid accumulation.
Conclusions:
- MRPL44 is identified as a novel regulator of lipid metabolism.
- MRPL44 demonstrates a protective role against MASLD via mitophagy.
- MRPL44 represents a potential therapeutic target for MASLD.
