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Helicobacter hepaticus promotes hepatic steatosis through CdtB-induced mitochondrial stress and lipid metabolism reprogramming
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Helicobacter hepaticus promotes hepatic steatosis through CdtB-induced mitochondrial stress and lipid metabolism reprogramming
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Journal Article
Helicobacter hepaticus promotes hepatic steatosis through CdtB-induced mitochondrial stress and lipid metabolism reprogramming
2025
Overview
Host-pathogen interaction influences many non-infectious diseases, including metabolic diseases.
Helicobacter hepaticus
(
H. hepaticus
) has been found in some metabolic dysfunction-associated steatotic liver disease (MASLD) patients, however, the causal link and underlying mechanisms remain unclear. Here we report that
H. hepaticus
infection or overexpression of CdtB of
H. hepaticus
induces lipid deposition in hepatocytes, both in vivo and in vitro. Furthermore, we identify that CdtB translocates to mitochondria with the help of Hsp90, interacts with ATP5A1, reduces mitochondrial respiratory complex V activity, damages mitochondria, and disrupts lipid metabolism. Mechanistically, CdtB-induced lipogenesis depends on the CdtB-mitochondrial ROS-mTORC1-SREBP1 axis and CdtB-mediated NONO expression to enhance nuclear localization of SREBP1 that promote the de novo fatty acid synthesis in the hepatocytes. Neutralization of CdtB significantly alleviates hepatic lipidosis in mice upon
H. hepaticus
infection. Furthermore, the nucleic acid of
H. hepaticus
has been detected in the liver tissues of some patients with MASLD, which suggests a certain correlation between liver infection with
H. hepaticus
and the occurrence and progression of MASLD. Our findings highlight the critical role of CdtB in the pathogenesis of
H. hepaticus
infection-induced hepatic lipidosis and its potential as a therapeutic target.
Here, the authors show that hepatic lipid accumulation induced by
Helicobacter hepaticus
involves mitochondrial dysfunction and disrupted lipid metabolism via CdtB-ROS-mTORC1-SREBP1 and NONO, highlighting CdtB as a key mediator and potential therapeutic target.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/1
/ 13/109
/ 13/31
/ 13/51
/ 13/95
/ 14/19
/ 14/28
/ 14/32
/ 64/60
/ Animals
/ Helicobacter hepaticus - genetics
/ Helicobacter hepaticus - metabolism
/ Helicobacter hepaticus - pathogenicity
/ Helicobacter Infections - complications
/ Helicobacter Infections - metabolism
/ Helicobacter Infections - microbiology
/ Helicobacter Infections - pathology
/ Humanities and Social Sciences
/ Humans
/ Lipids
/ Liver
/ Male
/ Mechanistic Target of Rapamycin Complex 1 - metabolism
/ Mice
/ Reactive Oxygen Species - metabolism
/ Science
/ Sterol Regulatory Element Binding Protein 1 - metabolism
/ Toxins
