ArticleLife medicine2022
Peroxisome proliferator-activated receptor γ coactivator 1α maintains NAD
Article in Life medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Hepatic Sirt2-PARP1-HMGB1 axis promotes exercise-mediated amelioration of MASH in mice.Science China. Life sciences · 2026Article
- Stem cell-based therapeutic strategies for liver aging.Liver research (Beijing, China) · 2025Review
- A single-nucleus transcriptomic atlas of primate liver aging uncovers the pro-senescence role of SREBP2 in hepatocytes.Protein & cell · 2024Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Epigenetic regulation of aging: implications for interventions of aging and diseases.Signal transduction and targeted therapy · 2022Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic metabolic derangements are pivotal incidences in the occurrence of hepatic steatosis, inflammation, and fibrosis. Peroxisome proliferator-activated receptor-γ, coactivator-1α (PGC-1α), a master regulator that mediates adipose metabolism and mitochondrial biogenesis, its role in hepatic steatosis and progression to steatohepatitis remains elusive. By surveying genomic data on nonalcoholic steatohepatitis (NASH) patients available in the Gene Expression Omnibus, we found that PGC-1α was significantly down-regulated compared with healthy controls, implicating the restoration of PGC-1α may ameliorate the hepatopathy. Using a hepatocyte-specific PGC-1α overexpression (LivPGC1α) mouse model, we demonstrated that PGC-1α attenuated hepatic steatosis induced by methionine-choline-deficient diet (MCD). Biochemical measurements and histological examination indicated less inflammatory infiltration, collagen deposition, NF-kB activation, and less lipid accumulation in LivPGC1α liver fed MCD. Further analyses indicated that the NAD
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Registered trials
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