Asset Details
Do you wish to reserve the book?
Transcriptome analysis of liver injury of fatty liver disease induced by ALDH2 deficiency
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Transcriptome analysis of liver injury of fatty liver disease induced by ALDH2 deficiency
Do you wish to request the book?
Transcriptome analysis of liver injury of fatty liver disease induced by ALDH2 deficiency
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Transcriptome analysis of liver injury of fatty liver disease induced by ALDH2 deficiency
2025
Overview
Aldehyde dehydrogenase 2 (
Aldh2
) Glu504Lys mutation, common in East Asians, is linked to various alcohol-related pathologies, notably fatty liver disease. Recent findings suggest that high ethanol-producing Klebsiella
pneumoniae
(HiAlc
Kpn
) exacerbates liver injury in non-alcoholic fatty liver disease (NAFLD). Our study investigated the combined effects of
Aldh2
deficiency and HiAlc
Kpn
on NAFLD liver injury, transcriptome analyses to unearth potential mechanisms and therapeutic targets. In our controlled experiment with
Aldh2
-deficient mice, we induced fatty liver via alcohol and HiAlc
Kpn
gavage, followed by comprehensive analyses to detect gene expression and epigenetic changes. The results showed that
Aldh2
-deficient mice were particularly vulnerable to ethanol and HiAlc
Kpn
, with notable gene expression changes in key metabolic and liver injury pathways. Our analysis identified crucial differentially expressed genes (DEGs) and pathways, highlighting the significant roles of genes like
Cyp8b1
,
Cyp7a1
, and
Ugt2b1
in liver metabolism and suggesting them as therapeutic targets. The study underscores the impact of
Aldh2
deficiency and HiAlc
Kpn
on NAFLD progression, revealing potential therapeutic strategies. Despite these insights, further research is needed to clarify the systemic effects on aldehyde metabolism and the full implications of
Aldh2
deficiency and HiAlc
Kpn
in liver injury.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ Aldehyde Dehydrogenase, Mitochondrial - deficiency
/ Aldehyde Dehydrogenase, Mitochondrial - genetics
/ Animals
/ DEGs
/ Ethanol
/ Humanities and Social Sciences
/ Liver
/ Male
/ Mice
/ Non-alcoholic Fatty Liver Disease - genetics
/ Non-alcoholic Fatty Liver Disease - metabolism
/ Non-alcoholic Fatty Liver Disease - pathology
/ Science
