ArticleResearch (Washington, D.C.)2023
Protective and Adverse Roles of DDX3X in Different Cell Types in Nonalcoholic Steatohepatitis Progression.
Article in Research (Washington, D.C.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- DDX3X overexpression in mice can cause rapid tissue-specific toxicity and mortality.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- E3 ubiquitin ligase trim36 targets ddx3x for degradation to reprogram macrophage polarization and ameliorate tubal factor infertility in rats.Cell biology and toxicology · 2026Article
- PGK1 Lactylation-Driven Self-Reinforcing Loop Orchestrates Glycolytic Reprogramming in FSP1Research (Washington, D.C.) · 2026Article
- Paeoniflorin Ameliorates Metabolic Dysfunction-Associated Steatotic Liver Disease by SYK/SH3BP2 Signaling Pathway.Research (Washington, D.C.) · 2026Article
- DDX3X/MAVS alleviates doxorubicin‑induced cardiotoxicity by regulating stress granules.Molecular medicine reports · 2025Article
- EVA1A Regulates Hepatic Lipid Homeostasis by Modulating CD36 Expression and Its Palmitoylation.Research (Washington, D.C.) · 2025Article
- Melatonergic Signaling Sustains Food Allergy Through FcεRI Recycling.Research (Washington, D.C.) · 2024Article
- Metabolic Dysfunction-Associated Steatohepatitis Detected by Neutrophilic Crown-Like Structures in Morbidly Obese Patients: A Multicenter and Clinicopathological Study.Research (Washington, D.C.) · 2024Article
- Hepatic Surf4 Deficiency Impairs Serum Amyloid A1 Secretion and Attenuates Liver Fibrosis in Mice.Research (Washington, D.C.) · 2024Article
- Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent hepatic cellular metabolic stress and liver inflammatory stimuli are key signatures of nonalcoholic steatohepatitis (NASH). DDX3X is a vital molecule involved in cell fate decisions in both pro-survival stress granule (SG) and pro-death NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome assembly in response to stress signals. However, the role of DDX3X in NASH remains unclear. We characterized the cell type-specific roles of DDX3X in NASH. Human liver tissues from NASH patients and normal control subjects were collected to assess DDX3X expression and distribution. Nutritional steatohepatitis models were constructed by feeding macrophage-specific DDX3X knockout (DDX3X
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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 OpenQuestion graph.