ArticleThe Journal of clinical investigation2011
Spontaneous hepatic repopulation in transgenic mice expressing mutant human α1-antitrypsin by wild-type donor hepatocytes.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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.
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Who cites it
45 citing papers in PubMed, 87 citations in OpenAlex.
- Cell therapy strategies for organ regeneration.BMC medicine · 2026Review
- From cold chain to ambient: Benefits, risks, and evidence across cell therapy logistics.Molecular therapy. Methods & clinical development · 2025Review
- Transient growth factor expression via mRNA in lipid nanoparticles promotes hepatocyte cell therapy in mice.Nature communications · 2024Article
- Liver directed adeno-associated viral vectors to treat metabolic disease.Journal of inherited metabolic disease · 2024Review
- Chemical approaches targeting the hurdles of hepatocyte transplantation: mechanisms, applications, and advances.Frontiers in cell and developmental biology · 2024Review
- Cell therapy in end-stage liver disease: replace and remodel.Stem cell research & therapy · 2023Review
- To not love thy neighbor: mechanisms of cell competition in stem cells and beyond.Cell death and differentiation · 2023Review
- Game of clones: Battles in the field of carcinogenesis.Pharmacology & therapeutics · 2022Review
- Review
- Hepatocyte organoids and cell transplantation: What the future holds.Experimental & molecular medicine · 2021Review
- Correction of a urea cycle defect after ex vivo gene editing of human hepatocytes.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Alpha-1 antitrypsin deficiency research and emerging treatment strategies: what's down the road?Therapeutic advances in chronic disease · 2021Review
- Treatment of α-1 antitrypsin deficiency using hepatic-specified cells derived from human-induced pluripotent stem cells.American journal of translational research · 2021Article
- [Research progress of hepatocyte transplantation treatment for alpha-1 antitrypsin deficiency].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- Emerging mechanisms of cell competition.Nature reviews. Genetics · 2020Review
- Alpha-1 Antitrypsin Deficiency-Mediated Liver Toxicity: Why Do Some Patients Do Poorly? What Do We Know So Far?Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Leveraging Population Genomics for Individualized Correction of the Hallmarks of Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Animal Models of Hepatitis C Virus Infection.Cold Spring Harbor perspectives in medicine · 2020Review
- Radiation-primed hepatocyte transplantation in murine monogeneic dyslipidemia normalizes cholesterol and prevents atherosclerosis.Journal of hepatology · 2019Article
- Hepatocyte Transplantation: Quo Vadis?International journal of radiation oncology, biology, physics · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
α1-Antitrypsin deficiency is an inherited condition that causes liver disease and emphysema. The normal function of this protein, which is synthesized by the liver, is to inhibit neutrophil elastase, a protease that degrades connective tissue of the lung. In the classical form of the disease, inefficient secretion of a mutant α1-antitrypsin protein (AAT-Z) results in its accumulation within hepatocytes and reduced protease inhibitor activity, resulting in liver injury and pulmonary emphysema. Because mutant protein accumulation increases hepatocyte cell stress, we investigated whether transplanted hepatocytes expressing wild-type AAT might have a competitive advantage relative to AAT-Z-expressing hepatocytes, using transgenic mice expressing human AAT-Z. Wild-type donor hepatocytes replaced 20%-98% of mutant host hepatocytes, and repopulation was accelerated by injection of an adenovector expressing hepatocyte growth factor. Spontaneous hepatic repopulation with engrafted hepatocytes occurred in the AAT-Z-expressing mice even in the absence of severe liver injury. Donor cells replaced both globule-containing and globule-devoid cells, indicating that both types of host hepatocytes display impaired proliferation relative to wild-type hepatocytes. These results suggest that wild-type hepatocyte transplantation may be therapeutic for AAT-Z liver disease and may provide an alternative to protein replacement for treating emphysema in AAT-ZZ individuals.
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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.