GSE201819: The genetic background shapes the susceptibility to mitochondrial dysfunction and NASH progression

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GROUP CONDITION SAMPLES
Liver
GSM6072156 GSM6072157 GSM6072166 GSM6072167 GSM6072194 GSM6072195 GSM6072196 GSM6072204 GSM6072210 GSM6072211 GSM6072212 GSM6072213 GSM6072214 GSM6072215 GSM6072216
GSM6072178 GSM6072179 GSM6072186 GSM6072187 GSM6072188 GSM6072189 GSM6072190 GSM6072191 GSM6072192 GSM6072193 GSM6072203
GSM6072205 GSM6072206 GSM6072207 GSM6072208 GSM6072209 GSM6072217 GSM6072218 GSM6072226 GSM6072227 GSM6072228 GSM6072229 GSM6072233 GSM6072234
GSM6072230 GSM6072231 GSM6072232 GSM6072235 GSM6072236 GSM6072237 GSM6072238 GSM6072239 GSM6072240 GSM6072241 GSM6072242 GSM6072243
GSM6072158 GSM6072159 GSM6072160 GSM6072161 GSM6072162 GSM6072163 GSM6072164 GSM6072165 GSM6072169 GSM6072170 GSM6072171 GSM6072181 GSM6072182 GSM6072183 GSM6072184 GSM6072185
GSM6072151 GSM6072152 GSM6072153 GSM6072154 GSM6072155 GSM6072168 GSM6072172 GSM6072173 GSM6072174 GSM6072175 GSM6072176 GSM6072177 GSM6072180
GSM6072197 GSM6072198 GSM6072199 GSM6072200 GSM6072201 GSM6072202 GSM6072219 GSM6072220 GSM6072221 GSM6072222 GSM6072223 GSM6072224 GSM6072225
Description

Submission Date: Apr 28, 2022

Summary: Non-alcoholic steatohepatitis (NASH) is a global health concern without treatment. The challenge in finding effective therapies is due to the lack of good mouse models and the complexity of the disease, characterized by gene–environment interactions. We tested the susceptibility of seven mouse strains to develop NASH. The severity of the clinical phenotypes observed varied widely across strains. PWK/PhJ mice were the most prone to develop hepatic inflammation and the only strain to progress to NASH with extensive fibrosis, while CAST/EiJ mice were completely resistant. Levels of mitochondrial transcripts and proteins as well as mitochondrial function were robustly reduced specifically in the liver of PWK/PhJ mice, suggesting a central role of mitochondrial dysfunction in NASH progression. Importantly, the NASH gene expression profile of PWK/PhJ mice had the highest overlap with the human NASH signature. Our study exposes the limitations of using a single mouse genetic background in metabolic studies and describes a novel NASH mouse model with features of the human NASH.

GEO Accession ID: GSE201819

PMID: 36787127

Description

Submission Date: Apr 28, 2022

Summary: Non-alcoholic steatohepatitis (NASH) is a global health concern without treatment. The challenge in finding effective therapies is due to the lack of good mouse models and the complexity of the disease, characterized by gene–environment interactions. We tested the susceptibility of seven mouse strains to develop NASH. The severity of the clinical phenotypes observed varied widely across strains. PWK/PhJ mice were the most prone to develop hepatic inflammation and the only strain to progress to NASH with extensive fibrosis, while CAST/EiJ mice were completely resistant. Levels of mitochondrial transcripts and proteins as well as mitochondrial function were robustly reduced specifically in the liver of PWK/PhJ mice, suggesting a central role of mitochondrial dysfunction in NASH progression. Importantly, the NASH gene expression profile of PWK/PhJ mice had the highest overlap with the human NASH signature. Our study exposes the limitations of using a single mouse genetic background in metabolic studies and describes a novel NASH mouse model with features of the human NASH.

GEO Accession ID: GSE201819

PMID: 36787127

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