ReviewMolecular genetics and metabolism2017
The liver is a metabolic and immunologic organ: A reconsideration of metabolic decompensation due to infection in inborn errors of metabolism (IEM).
Review in Molecular genetics and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- L-Carnitine Prevents Lipopolysaccharide-Induced Inflammatory Response, Microglia Activation and Neuronal Damage in Cerebral Cortex, as Well as Neuromotor Development Delay in Neonatal Glutaryl-CoA Dehydrogenase Deficient (GcdhJournal of inherited metabolic disease · 2026Article
- Hepatic transcriptomics reveals immuno-metabolic interactions in juvenile channel catfish (Ictalurus punctatus) after Aeromonas hydrophila infection.BMC genomics · 2026Article
- The ADAM Family of Proteases: Structure, Substrates, and Roles in Liver Diseases.International journal of molecular sciences · 2026Review
- The gut-liver axis modulates intestinal immune homeostasis.Mucosal immunology · 2026Review
- Integrative bioinformatics analysis identifies APOE as a candidate link between lipid dysregulation and macrophage activation in inborn errors of metabolism.Frontiers in pharmacology · 2026Article
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Perspectives of pediatric patients with inborn errors of metabolism on long-term treatment and metabolic emergency management.Orphanet journal of rare diseases · 2025Article
- Clinical burden of propionic acidemia in the United States: a claims-based study by age stratum.Orphanet journal of rare diseases · 2025Article
- Effects of Dairy Matrix on the Intestinal, Liver, and Bone Transcriptome of Healthy Rats.Foods (Basel, Switzerland) · 2025Article
- Functional overlap of inborn errors of immunity and metabolism genes defines T cell metabolic vulnerabilities.Science immunology · 2024Article
- Article
- Epitope-level profiling in children with mitochondrial disease reveals limitations in the antibacterial antibody repertoire.Molecular genetics and metabolism · 2023Article
- Advances in the pharmacological effects and molecular mechanisms of emodin in the treatment of metabolic diseases.Frontiers in pharmacology · 2023Review
- Comprehensive profiling of the human viral exposome in households containing an at-risk child with mitochondrial disease during the 2020-2021 COVID-19 pandemic.Clinical and translational medicine · 2022Article
- The potential and limitations of intrahepatic cholangiocyte organoids to study inborn errors of metabolism.Journal of inherited metabolic disease · 2022Article
- The clinical spectrum of SARS-CoV-2 infection in Gaucher disease: Effect of both a pandemic and a rare disease that disrupts the immune system.Molecular genetics and metabolism · 2022Observational
- Article
- Single-cell analysis reveals the intra-tumor heterogeneity and identifies MLXIPL as a biomarker in the cellular trajectory of hepatocellular carcinoma.Cell death discovery · 2021Article
- Prognostic Implication of a Novel Metabolism-Related Gene Signature in Hepatocellular Carcinoma.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Metabolic decompensation in inborn errors of metabolism (IEM) is characterized by a rapid deterioration in metabolic status leading to life-threatening biochemical perturbations (e.g. hypoglycemia, hyperammonemia, acidosis, organ failure). Infection is the major cause of metabolic decompensation in patients with IEM. We hypothesized that activation of the immune system during infection leads to further perturbations in end-organ metabolism resulting in increased morbidity. To address this, we established model systems of metabolic decompensation due to infection. Using these systems, we have described the pathologic mechanisms of metabolic decompensation as well as changes in hepatic metabolic reserve associated with infection. First and foremost, our studies have demonstrated that the liver experiences a significant local innate immune response during influenza infection that modulates hepatic metabolism. Based on these findings, we are the first to suggest that the role of the liver as a metabolic and immunologic organ is central in the pathophysiology of metabolic decompensation due to infection in IEM. The dual function of the liver as a major metabolic regulator and a lymphoid organ responsible for immunosurveillance places this organ at risk for hepatotoxicity. Mobilization of hepatic reserve and the regenerative capacity of a healthy liver compensates for this calculated risk. However, activation of the hepatic innate immune system may be deleterious in IEM. Based on this assertion, strategies aimed at modulating the innate immune response may be a viable target for intervention in the treatment of hepatic metabolic decompensation.
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