ArticleScientific reports2019
The Differential Expression of Cide Family Members is Associated with Nafld Progression from Steatosis to Steatohepatitis.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- A Distinctive NAFLD Signature in Adipose Tissue from Women with Severe Obesity.International journal of molecular sciences · 2021Trial
- Longevity-driven hepatic transcriptional programs mediate resilience to diet-induced liver injury in Ames dwarf mice.GeroScience · 2026Article
- Fatty acid-activated proton transporter SR4 prevents hepatic steatosis and metabolic alterations in diabetic mice by improving mitochondria function, energy balance and oxidative stress.Experimental and therapeutic medicine · 2026Article
- METTL16 promotes MASLD progression through the regulation of lipid synthesis and immune response.Biology direct · 2026Article
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes.Clinical and molecular hepatology · 2026Article
- Cell death-inducing DNA fragmentation factor alpha (DFFA)-like effectors (CIDEs) improve lipid droplet (LD) formation and oil accumulation in plant tissues.Plant biotechnology journal · 2025Article
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- Administration of heat killed Fructobacillus fructosus OS-1010 attenuates metabolic disease induced by high fat diet in mice.Scientific reports · 2025Article
- CIDEB promotes lipid deposition in goat intramuscular adipocytes.Animal bioscience · 2025Article
- LncRNAeLife · 2024Article
- Elongation factor 1A1 inhibition elicits changes in lipid droplet size, the bulk transcriptome, and cell type-associated gene expression in MASLD mouse liver.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Targeting lipid droplets and lipid droplet-associated proteins: a new perspective on natural compounds against metabolic diseases.Chinese medicine · 2024Review
- Spatial and single-cell profiling of the metabolome, transcriptome and epigenome of the aging mouse liver.Nature aging · 2023Article
- Sterile inflammation in liver transplantation.Frontiers in medicine · 2023Review
- Moderate Treadmill Exercise Alleviates NAFLD by Regulating the Biogenesis and Autophagy of Lipid Droplet.Nutrients · 2022Article
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- Systematic Analysis of Long Non-Coding RNA Genes in Nonalcoholic Fatty Liver Disease.Non-coding RNA · 2022Article
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- METTL16-mediated translation ofPeerJ · 2022Article
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Improved understanding of the molecular mechanisms responsible for the progression from a "non-pathogenic" steatotic state to Non-Alcoholic Steatohepatitis is an important clinical requirement. The cell death-inducing DFF45 like effector (CIDE) family members (A, B and FSP27) regulate hepatic lipid homeostasis by controlling lipid droplet growth and/or VLDL production. However, CIDE proteins, particularly FSP27, have a dual role in that they also regulate cell death. We here report that the hepatic expression of CIDEA and FSP27 (α/β) was similarly upregulated in a dietary mouse model of obesity-mediated hepatic steatosis. In contrast, CIDEA expression decreased, but FSP27-β expression strongly increased in a dietary mouse model of steatohepatitis. The inverse expression pattern of CIDEA and FSP27β was amplified with the increasing severity of the liver inflammation and injury. In obese patients, the hepatic CIDEC2 (human homologue of mouse FSP27β) expression strongly correlated with the NAFLD activity score and liver injury. The hepatic expression of CIDEA tended to increase with obesity, but decreased with NAFLD severity. In hepatic cell lines, the downregulation of FSP27β resulted in the fractionation of lipid droplets, whereas its overexpression decreased the expression of the anti-apoptotic BCL2 marker. This, in turn, sensitized cells to apoptosis in response to TNF α and saturated fatty acid. Considered together, our animal, human and in vitro studies indicate that differential expression of FSP27β/CIDEC2 and CIDEA is related to NAFLD progression and liver injury.
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