ArticleAntioxidants (Basel, Switzerland)2021
Cisd2 Protects the Liver from Oxidative Stress and Ameliorates Western Diet-Induced Nonalcoholic Fatty Liver Disease.
Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- NAFLD and Hypothyroidism: Deciphering Pivotal Genetic Variants, Cellular Expression Landscapes, and Spatial Architectures.International journal of molecular sciences · 2026Article
- CISD2 ensures adequate ER-mitochondrial coupling, critically supporting mitochondrial function in neurons.Acta neuropathologica communications · 2025Article
- The role of mitophagy in female reproductive system diseases: from molecular mechanisms to therapeutic strategies.Frontiers in endocrinology · 2025Review
- Article
- NUP85 alleviates lipid metabolism and inflammation by regulating PI3K/AKT signaling pathway in nonalcoholic fatty liver disease.International journal of biological sciences · 2024Article
- From gut to liver: unveiling the differences of intestinal microbiota in NAFL and NASH patients.Frontiers in microbiology · 2024Article
- Article
- Upregulation of CDGSH iron sulfur domain 2 attenuates cerebral ischemia/reperfusion injury.Neural regeneration research · 2023Article
- Rejuvenation: Turning Back Time by Enhancing CISD2.International journal of molecular sciences · 2022Review
- Inhibition of CISD2 promotes ferroptosis through ferritinophagy-mediated ferritin turnover and regulation of p62-Keap1-NRF2 pathway.Cellular & molecular biology letters · 2022Article
- Dysregulated CaCells · 2022Review
- Article
- Cisd2 Preserves the Youthful Pattern of the Liver Proteome during Natural Aging of Mice.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) and its more severe form, nonalcoholic steatohepatitis (NASH), are the most common chronic liver diseases worldwide. However, drugs to treat NAFLD and NASH are an unmet clinical need. This study sought to provide evidence that Cisd2 is a molecular target for the development of treatments targeting NAFLD and NASH. Several discoveries are pinpointed. The first is that Cisd2 dosage modulates the severity of Western diet-induced (WD-induced) NAFLD. Specifically, Cisd2 haploinsufficiency accelerates NAFLD development and exacerbates progression toward NASH. Conversely, an enhanced Cisd2 copy number attenuates liver pathogenesis. Secondly, when a WD is fed to mice, transcriptomic analysis reveals that the major alterations affecting biological processes are related to inflammation, lipid metabolism, and DNA replication/repair. Thirdly, among these differentially expressed genes, the most significant changes involve Nrf2-mediated oxidative stress, cholesterol biosynthesis, and fatty acid metabolism. Finally, increased Cisd2 expression protects the liver from oxidative stress and reduces the occurrence of mitochondrial DNA deletions. Taken together, our mouse model reveals that Cisd2 plays a crucial role in protecting the liver from WD-induced damages. The development of therapeutic agents that effectively enhance Cisd2 expression is one potential approach to the treatment of WD-induced fatty liver diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.