ArticleJournal of autoimmunity2023
mTOR-dependent loss of PON1 secretion and antiphospholipid autoantibody production underlie autoimmunity-mediated cirrhosis in transaldolase deficiency.
Article in Journal of autoimmunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.
- Liver Disease in Transaldolase Deficiency: Molecular Basis, Genotype-Phenotype Relationships, and Transplantation Outcomes-A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Genetic determinants of arterial thrombosis in primary antiphospholipid syndrome: a systematic review.Frontiers in immunology · 2026Pooled it
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- The Prevalence of Anemia and Diagnostic Usefulness of Ferritin and Hepcidin in Antiphospholipid Syndrome and Systemic Lupus Erythematosus Patients.Diseases (Basel, Switzerland) · 2026Article
- Long-Term Follow-Up of Patients With Transaldolase Deficiency.Journal of inherited metabolic disease · 2026Article
- Circ_0039857: A Key Player in Combating Immune Disorders and Ferroptosis in High-Glucose-induced HK-2 Cells and Diabetic Kidney Disease Mice.Applied biochemistry and biotechnology · 2026Article
- Microbiome and metabolite signatures for cirrhosis to HCC risk stratification: progress, controversies, and gaps.Frontiers in cellular and infection microbiology · 2026Review
- Matrix Metalloproteinase-9 (MMP-9) as a Therapeutic Target: Insights into Molecular Pathways and Clinical Applications.Pharmaceutics · 2025Review
- Molecular network of metabolic reprogramming and precision diagnosis and treatment of hepatocellular carcinoma.Biomarker research · 2025Review
- Features and Prognosis of Patients With Retroperitoneal Fibrosis Developing Fibrosing Mediastinitis: Case-Control Study and Systematic Review.ACR open rheumatology · 2025Article
- Review
- Overview of Oxidative Stress in Systemic Lupus Erythematosus.Antioxidants (Basel, Switzerland) · 2025Review
- Gluconolactone restores immune regulation and alleviates skin inflammation in lupus-prone mice and in patients with cutaneous lupus.Science translational medicine · 2025Article
- Identification of immune and major depressive disorder-related diagnostic markers for early nonalcoholic fatty liver disease by WGCNA and machine learning.Frontiers in bioinformatics · 2025Article
- Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024Review
- The hepatocellular carcinoma risk in patients with HBV-related cirrhosis: a competing risk nomogram based on a 4-year retrospective cohort study.Frontiers in oncology · 2024Article
- Reprogramming of regulatory T cells in inflammatory tumor microenvironment: can it become immunotherapy turning point?Frontiers in immunology · 2024Review
- B and T cells: (Still) the dominant orchestrators in autoimmune hepatitis.Autoimmunity reviewsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
Transaldolase deficiency predisposes to chronic liver disease progressing from cirrhosis to hepatocellular carcinoma (HCC). Transition from cirrhosis to hepatocarcinogenesis depends on mitochondrial oxidative stress, as controlled by cytosolic aldose metabolism through the pentose phosphate pathway (PPP). Progression to HCC is critically dependent on NADPH depletion and polyol buildup by aldose reductase (AR), while this enzyme protects from carbon trapping in the PPP and growth restriction in TAL deficiency. Although AR inactivation blocked susceptibility to hepatocarcinogenesis, it enhanced growth restriction, carbon trapping in the non-oxidative branch of the PPP and failed to reverse the depletion of glucose 6-phosphate (G6P) and liver cirrhosis. Here, we show that inactivation of the TAL-AR axis results in metabolic stress characterized by reduced mitophagy, enhanced overall autophagy, activation of the mechanistic target of rapamycin (mTOR), diminished glycosylation and secretion of paraoxonase 1 (PON1), production of antiphospholipid autoantibodies (aPL), loss of CD161
Indexed as
Identifiers
What OpenQuestion holds
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.