ArticleCells2018
Retinoids Issued from Hepatic Stellate Cell Lipid Droplet Loss as Potential Signaling Molecules Orchestrating a Multicellular Liver Injury Response.
Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Curcumin Targets Crispld2 to Suppress Hepatic Stellate Cell Activation via PI3K/AKT Pathway Inhibition in Hepatic Fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- RXRActa pharmaceutica Sinica. B · 2025Article
- Nitric oxide donor S-Nitroso-N-acetyl penicillamine for hepatic stellate cells to restore quiescence.Pediatric discovery · 2024Article
- Dysfunction of autophagy in high-fat diet-induced non-alcoholic fatty liver disease.Autophagy · 2024Review
- Eupatilin Ameliorates Hepatic Fibrosis and Hepatic Stellate Cell Activation by Suppressing β-catenin/PAI-1 Pathway.International journal of molecular sciences · 2023Article
- Review
- Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023Review
- MAFLD: a multisystem disease.Therapeutic advances in endocrinology and metabolism · 2023Review
- The role of hepatic microenvironment in hepatic fibrosis development.Annals of medicine · 2022Review
- Mechanisms of Xiaochaihu Decoction on Treating Hepatic Fibrosis Explored by Network Pharmacology.Disease markers · 2022Article
- Targeting fatty acid metabolism for fibrotic disorders.Archives of pharmacal research · 2021Review
- Cellular and molecular effects of silymarin on the transdifferentiation processes of LX-2 cells and its connection with lipid metabolism.Molecular and cellular biochemistry · 2020Article
- Assessment of Genetic Aspects of Non-alcoholic Fatty Liver and Premature Cardiovascular Events.Middle East journal of digestive diseases · 2020Review
- Lipid Droplets and the Management of Cellular Stress.The Yale journal of biology and medicine · 2019Review
- Lipid Droplets in Disease.Cells · 2019Article
- Cellular and molecular effects of Baccharis dracunculifolia D.C. and Plectranthus barbatus Andrews medicinal plant extracts on retinoid metabolism in the human hepatic stellate cell LX-2.BMC complementary and alternative medicine · 2019Article
- Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis.Cell death & disease · 2019Review
- Hepatic stellate cells - from past till present: morphology, human markers, human cell lines, behavior in normal and liver pathology.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hepatic stellate cells (HSCs) serve as the main body storage compartment for vitamin A through retinyl ester (RE)-filled lipid droplets (LDs). Upon liver injury, HSCs adopt a myofibroblastic phenotype characterized by an elevated expression of extracellular matrix proteins and a concomitant loss of LDs. On the one hand, LD breakdown has been suggested to provide the energy required for HSC activation into myofibroblast-like cells. On the other hand, this process could mitigate HSC activation following the transformation of released REs into retinoic acids (RAs), ligands for nuclear receptors exerting antifibrotic transcriptional regulatory activities in HSCs. Importantly, RAs may also constitute a means for HSCs to orchestrate the liver response to injury by triggering transcriptional effects in multiple additional surrounding liver cell populations. We envision that new approaches, such as single-cell technologies, will allow to better define how RAs are issued from LD loss in HSCs exert a multicellular control of the liver (patho)physiology.
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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.