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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature non-alcoholic fatty liver disease (NAFLD) is characterized by liver fat accumulation of more than 5%, which has become the most common liver disease and affects 25% of the global population.
Despite a lot of research, the molecular mechanism of NAFLD has not been fully elucidated, and there is a lack of complete drug treatment methods.
On April 24, 2021, Zhe Zhigang, Li Hongliang and Hu Yufeng of Wuhan University jointly published a research paper entitled "Hepatocyte SH3RF2 Deficiency is a Key Aggravator for Nonalcoholic Fatty Liver Disease" in Hepatology (IF=14.
68).
The research found SH3RF2 is inhibited in NAFLD in mice, monkeys and clinical individuals.
Based on the gene interference model, this study further proved that hepatocyte SH3RF2 significantly reduced lipid accumulation in cultured hepatocytes and diet-induced NAFLD mice.
In terms of mechanism, SH3RF2 directly binds to ATP citrate lyase (ACLY), which is the main enzyme that promotes the production of cytosolic acetyl-CoA and promotes its ubiquitination-dependent degradation linked to K48.
Consistently, compared with the wild-type control, the Sh3rf2 knockout hepatocytes and liver accumulated a large amount of acetyl-CoA, which resulted in de novo fat formation, increased cholesterol production, and increased lipid deposition.
In conclusion, the study found that SH3RF2 depletion in liver cells is a key aggravating factor in the progression of NAFLD, which represents a promising therapeutic target for related liver diseases.
In addition, on April 7, 2021, Zhe Zhigang and Li Hongliang of Wuhan University jointly published a review article entitled "Therapeutic Potential of G Protein-Coupled Receptors against Nonalcoholic Steatohepatitis" in Hepatology.
The review analyzed the latest GPCR in NASH.
Report and discuss the trend of using GPCRs as therapeutic targets for NASH (click to read).
In 2020, Li Hongliang's team at Wuhan University published more than 20 high-level research results (click to read).
Non-alcoholic fatty liver disease (NAFLD) is characterized by liver fat accumulation of more than 5%, which has become the most common liver disease and affects 25% of the global population.
In terms of etiology, NAFLD is closely related to systemic metabolic abnormalities.
Systemic metabolic abnormalities usually include obesity, insulin resistance, hyperglycemia and dyslipidemia.
Excessive lipid deposition has been thought to be the cause of the progression of NAFLD.
In more than 25% of NAFLD patients, the disease further develops into non-alcoholic steatohepatitis (NASH), which greatly increases the risk of hepatocellular carcinoma (HCC) and extrahepatic cardiovascular disease.
Despite extensive research, the molecular mechanism of NAFLD has not yet been fully elucidated, and FDA-approved pharmacological strategies for NAFLD have not yet been established.
Protein degradation based on ubiquitination has recently become an attractive treatment strategy for human diseases, and such drugs are undergoing clinical development in cancer research.
However, this treatment strategy has not been applied to NAFLD.
In the multi-step process of protein degradation based on ubiquitination, E3 ligase represents the core regulator.
Members of the subfamily containing a RING domain are the main subunits of E3 ligase and act as a scaffold that regulates the direct transfer of ubiquitin from E2 to the substrate.
In recent years, SH3 domain-containing ring finger 2 (SH3RF2, also known as POSHER) has been identified as a new RING E3 ligase, and is involved in apoptosis, survival and differentiation of many cell types.
However, the function of SH3RF2 in the progression of hepatocytes and NAFLD is still unknown.
In this study, a significant down-regulation of SH3RF2 in non-alcoholic fatty liver was found.
The lack of Sh3rf2 in liver cells can enhance lipid accumulation in liver cells and cause diet-induced NAFLD.
It is worth noting that this study provides the first evidence supporting SH3RF2 as a novel E3 ligase to promote ubiquitination and degradation of ATP citrate lyase (ACLY).
The findings of this study provide new treatment goals and strategies for NAFLD.
Reference message: https://aasldpubs.
onlinelibrary.
wiley.
com/doi/10.
1002/hep.
31863
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature non-alcoholic fatty liver disease (NAFLD) is characterized by liver fat accumulation of more than 5%, which has become the most common liver disease and affects 25% of the global population.
Despite a lot of research, the molecular mechanism of NAFLD has not been fully elucidated, and there is a lack of complete drug treatment methods.
On April 24, 2021, Zhe Zhigang, Li Hongliang and Hu Yufeng of Wuhan University jointly published a research paper entitled "Hepatocyte SH3RF2 Deficiency is a Key Aggravator for Nonalcoholic Fatty Liver Disease" in Hepatology (IF=14.
68).
The research found SH3RF2 is inhibited in NAFLD in mice, monkeys and clinical individuals.
Based on the gene interference model, this study further proved that hepatocyte SH3RF2 significantly reduced lipid accumulation in cultured hepatocytes and diet-induced NAFLD mice.
In terms of mechanism, SH3RF2 directly binds to ATP citrate lyase (ACLY), which is the main enzyme that promotes the production of cytosolic acetyl-CoA and promotes its ubiquitination-dependent degradation linked to K48.
Consistently, compared with the wild-type control, the Sh3rf2 knockout hepatocytes and liver accumulated a large amount of acetyl-CoA, which resulted in de novo fat formation, increased cholesterol production, and increased lipid deposition.
In conclusion, the study found that SH3RF2 depletion in liver cells is a key aggravating factor in the progression of NAFLD, which represents a promising therapeutic target for related liver diseases.
In addition, on April 7, 2021, Zhe Zhigang and Li Hongliang of Wuhan University jointly published a review article entitled "Therapeutic Potential of G Protein-Coupled Receptors against Nonalcoholic Steatohepatitis" in Hepatology.
The review analyzed the latest GPCR in NASH.
Report and discuss the trend of using GPCRs as therapeutic targets for NASH (click to read).
In 2020, Li Hongliang's team at Wuhan University published more than 20 high-level research results (click to read).
Non-alcoholic fatty liver disease (NAFLD) is characterized by liver fat accumulation of more than 5%, which has become the most common liver disease and affects 25% of the global population.
In terms of etiology, NAFLD is closely related to systemic metabolic abnormalities.
Systemic metabolic abnormalities usually include obesity, insulin resistance, hyperglycemia and dyslipidemia.
Excessive lipid deposition has been thought to be the cause of the progression of NAFLD.
In more than 25% of NAFLD patients, the disease further develops into non-alcoholic steatohepatitis (NASH), which greatly increases the risk of hepatocellular carcinoma (HCC) and extrahepatic cardiovascular disease.
Despite extensive research, the molecular mechanism of NAFLD has not yet been fully elucidated, and FDA-approved pharmacological strategies for NAFLD have not yet been established.
Protein degradation based on ubiquitination has recently become an attractive treatment strategy for human diseases, and such drugs are undergoing clinical development in cancer research.
However, this treatment strategy has not been applied to NAFLD.
In the multi-step process of protein degradation based on ubiquitination, E3 ligase represents the core regulator.
Members of the subfamily containing a RING domain are the main subunits of E3 ligase and act as a scaffold that regulates the direct transfer of ubiquitin from E2 to the substrate.
In recent years, SH3 domain-containing ring finger 2 (SH3RF2, also known as POSHER) has been identified as a new RING E3 ligase, and is involved in apoptosis, survival and differentiation of many cell types.
However, the function of SH3RF2 in the progression of hepatocytes and NAFLD is still unknown.
In this study, a significant down-regulation of SH3RF2 in non-alcoholic fatty liver was found.
The lack of Sh3rf2 in liver cells can enhance lipid accumulation in liver cells and cause diet-induced NAFLD.
It is worth noting that this study provides the first evidence supporting SH3RF2 as a novel E3 ligase to promote ubiquitination and degradation of ATP citrate lyase (ACLY).
The findings of this study provide new treatment goals and strategies for NAFLD.
Reference message: https://aasldpubs.
onlinelibrary.
wiley.
com/doi/10.
1002/hep.
31863
